ملازم د.زهير

University of Kufa Microbiology
College of Dentistry 2019-2020 3rd Class

Lecture 2 Prof. Dr. Zuhair Alsehlawi
Ecology of Normal Microbial Flora
Ecology is a wide range term indicates to the science that study of interactions among
organisms and their abiotic environment. Ecosystem processes, such as primary
production, nutrient cycling, and various niche construction activities, regulate the
flux of energy and matter through an environment. Micro niche is a term describing
the way of life of a species.
The Nature of Host-parasite Interactions in Humans
Bacteria that are consistently associated with a human are called the normal flora.
These bacteria have a full range of symbiotic interactions with their hosts. In
biology, symbiosis is defined as "life together", A close and often long-term relation
that two organisms live in an association with one-another. Thus, there are at least
four types of relationships based on the quality of the association for the members of
the symbiotic association.
1. Mutualism: Both members of the association are benefit. This is a type of

synergism relationship.
2. Commensalism: There is no apparent benefit or harm to either member of the
association or one is benefit without affecting the other.
3. Parasitism: One member of the association lives or benefits at the expense of the
other member. This is a type of antagonism relationship.
4. Opportunistic Pathogen: A commensal organism which no harm under normal
condition. But it able to cause disease in certain circumstances (Staphylococcus
aureus, Clostridium difficile and Candida albicans cause infections to the host with
a weakened immune system).
The term "normal microbial flora" denotes the population of microorganisms that
inhabit the skin and mucous membranes of healthy normal persons (in healthy body
the internal tissues, e.g. blood, brain, muscle, etc., are normally free of
microorganisms). The skin and mucous membranes always harbor a variety of
microorganisms that can be arranged into two groups:
(1) The resident flora (indigenous microbiota) consists of relatively fixed types of
microorganisms regularly found in a given area at a given age. It has an important
functions in the host including: digestion, nutrition and competition with pathogenic
bacteria.
(2) The transient flora (Exogenous microbiota) consists of nonpathogenic or

potentially pathogenic microorganisms that inhabit the skin or mucous membranes for
hours, days, or weeks; it is derived from the environment.
Normal Flora of the Human Oral Cavity.
The presence of nutrients, epithelial debris, and vital secretions make the mouth a
favorable habitat for a great variety of microbes. Oral microflora refers to the
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community of microorganisms coexisting in the oral cavity as its primary habitat and
communicate between each other through complex cell signaling processes (Fig. 1).
Ecology of oral cavity
The mouth presents a succession of different ecological situations with human age,
and this corresponds with changes in the composition of the normal flora.
1- Infancy the oral cavity is composed solely of the soft tissues of the lips,
cheeks, tongue and palate, which are kept moist by the secretions of the
salivary glands. Ecosystem classified into the following:
a- At birth, the oral cavity is sterile but rapidly becomes colonized from the
environment, particularly from the mother (vertical transmission) in the
first feeding. Streptococcus salivarius is dominant and may make up 98%
of the total oral flora until the appearance of the teeth (6-9 months in
humans).
b- The neonatal period: Mostly aerobes and Candida albicans (54%) are
present .
c- Period before eruption: Colonized by facultative anaerobes and anaerobes;
Streptococcus (90%) ; Actinomyces and Candida albicans.
2- During the first year (The eruption of the teeth) the individual is further
exposed to external sources of bacteria (Horizontal transmission) and the
biodiversity of the oral cavity increases that leads to colonization by
Streptococcus. mutans and Streptococcus sanguis. These bacteria require a non
epithelial surface in order to colonize. Other strains of Streptococci adhere
strongly to the gums and cheeks but not to the teeth.
3- Over time as The creation of the gingival crevice area (supporting structures
of the teeth) increases the habitat for the variety of anaerobic species found
Actinomyces; Lactobacillus; Veillonella; Fusiform; Spirochetes. The
complexity of the oral flora continues to increase around puberty.
4- Elderly when complete loss of teeth shifts flora towards infant state.
In general, there are three explanations for why the normal bacterial flora are
located at particular anatomical sites.
1. Tissue tropism The normal flora exhibit a tissue preference or predilection for
colonization. One explanation for tissue tropism is that the host provides an
essential growth factor needed by the bacterium.
2. Colonize a particular tissue Perhaps most, of the normal flora are able to
colonize surface using their own surface components (e.g. capsules, fimbriae,
cell wall components, etc.) as specific ligands for attachment to specific
receptors located at the colonization site
3. Construct bacterial biofilms Some of the indigenous bacteria are able to on a
tissue surface, or they are able to colonize a biofilm built by another bacterial
species.
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Factors Affecting Growth of Microorganisms in the oral cavi1.
1-Temperature: Relatively constant 34˚-36 allows a large number of

microorganisms are variable on the teeth and mucosa.
2. REDOX Potential Eh: These processes depend on the oxygen during

enzymatic oxidation reduction reactions. In a predominance of reduction
processes have a negative redox potential and develop anaerobic
microorganisms are proximal surfaces and gingival crevice, while, positive
redox potential are buccal and palatal mucosa and the back part of the tongue.
The redox potential has been shown to fall during plaque development on a
clean enamel surface from an initial Eh of over +200 mV (highly oxidized) to
–141 mV (highly reduced) after 7 days. The development of plaque in this
way is associated with a specific succession of colonizing microorganisms.
Early colonizers will utilize O2 and produce CO2; later colonizers may
produce H2 and other reducing agents such as sulphur-containing compounds
and volatile fermentation products. Thus, as the Eh is gradually lowered, sites
become suitable for the survival and growth of a changing pattern of
organisms, and particularly obligate anaerobes.
— 3. pH: In the mouth pH varies between 6.7 and 7.3. It is maintained by saliva
through flow rate and buffer system. micrflora depending on pH of eco niches
(surrounding micro environment).
—
— 4. Nutrients: Including: dead epithelial cells, gingival fluid; Saliva, residues
from host`s , and products of metabolism of other microbial species
—
— 5. Host Defenses : Majority of organism removed by washing or by
nonspecific factors like antimicrobial factors (mucin, lysozyme and
lactoferrin) and specific protection eg. IgA.
—
— 6. Host genetics : Changes in immune response etc.
7. Antimicrobial agents: Antibiotics suppress the resident microflora, leading

to over-development of antibiotic resistant species and allow colonization of
exogenous pathogens such as Enterobacteriaceae.
The oral flora and causes oral diseases
Abscesses, dental caries, gingivitis, and periodontal disease; If oral

bacteria can gain entrance into deeper tissues, they may cause abscesses of
alveolar bone, lung, brain, If oral streptococci are introduced into wounds
created by dental manipulation or treatment, they may adhere to heart valves
and initiate subacute bacterial endocarditis.
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The Benefits of the Normal flora
Following are the primary beneficial effects of the normal flora.

1. Normal flora synthesize and excrete vitamins: For example, enteric
bacteria secrete Vitamin K and Vitamin B12, and lactic acid bacteria produce
certain B-vitamins.
2. Normal flora prevent colonization by pathogens by competing for

attachment sites or for essential nutrients.
3. Normal flora may antagonize other bacteria through the production of

substances which inhibit or kill non indigenous species. Like hydrogen
peroxide and bacteriocins, which inhibit or kill other bacteria.
4. Normal flora stimulate the development of certain tissues, i.e., the

caecum and certain lymphatic tissues (Peyer's patches) in the GI tract. based
on the ability to undergo immunological stimulation.
5. Normal flora stimulate the production of cross-reactive antibodies.

Since the normal flora behave as antigens, they induce an immunological
response, in particular, an antibody-mediated immune (AMI) response. Low
levels of antibodies produced against components of the normal flora are
known to cross react with certain related pathogens, and thereby prevent
infection or invasion. Antibodies produced against antigenic components of
the normal flora are sometimes referred to as "natural" antibodies.
6. Normal flora achieved colonization resistance through the saturation of

oral surfaces with preexisting resident bacteria, which reduces the available
sites left for the attachment of exogenous organisms.
Figure 1: Distribution of the microflora at distinct sites in the mouth.
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College of Dentistry 2019-2020 3 rd Class
DENTAL CARIES AND PERIODONTAL INFECTIONS

Dental plaque, dental caries and periodontitis are arguably the most significant and
costly negative effect resulting from human symbioses with normal bacterial flora.
Dental Plaque:
All materials that adhering to the teeth, consists of bacterial cells (60-70% the
volume of the plaque), salivary polymers, and bacterial extracellular products (figure
2). Plaque is a naturally-constructed biofilm, in which the bacteria may reach a
thickness of 300-500 cells on the surfaces of the teeth. These accumulations subject
the teeth and gingival tissues to high concentrations of bacterial metabolites, which
result in dental disease. By far the dominant bacterial species in dental plaque are
Streptococcus sanguis and Streptococcus mutans, both of which are considered
responsible for plaque.
Plaque Formation: Three steps are involved in the formation of dental plaque;
1- First salivary molecules are adsorbed to the enamel as soon as a tooth has been
cleaned. Hence the enamel is coated with a complex mixture of components
that include glycoproteins, acidic proline-rich proteins, mucins, bacterial cell
debris, exoproducts, and sialic acid.
2- The second step is bacterial interaction with this acquired pellicle via several
specific cell-to-surface interactions. Plaque is initiated by a weak attachment
of the primary colonizers, mainly Streptococcus sanguis and Actinomyces
viscosus, is influenced by a number of environmental parameters, such as
osmolarity, carbon source, and pH.
3- During the third step, other bacterial species like S. mutans adhere to the
primary colonizers by cell-to-cell interactions. Subsequent bacterial growth on
tooth surface leads to formation of biofilm on the teeth. A stronger attachment
by means of extracellular sticky polymers (glucans) which are synthesized by
the bacteria from dietary sugars (principally sucrose).
An increase in dietary carbohydrates, particularly sucrose, results in additional acid
production that may frequent exceed acidification of the plaque .
Role of Oral Streptococci in The Formation of Extracellular Polysaccharides

The acidogenic S. mutans and S. sobrinus are able to form extracellular
polysaccharides (EPS) in the presence of sucrose, but also from fructose and glucose.
The EPS are long-chained and high molecular mass polymers. The energy rich
glycosidic bond between the glucose and fructose moieties supplies the free energy
needed for the synthesis of EPS. Glucose homopolysaccharides are called glucans
while fructose homopolysaccharides are called fructans. Glucans are produced by
glucosyltransferases (GTF) while fructans are produced by fructosyltransferases
(FTF). The production of large quantities of EPSs from sucrose is an important factor
of S. mutans cariogenicity EPSs have progress affecting on dental caries has been
described as follows :
1- polysaccharides provide reserve of substrates.
2- EPSs aid adherence.
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3- water-insoluble EPSs act as diffusion barriers thus trapping acid near the tooth
surface.
4- EPSs increase the plaque thickness and thus acid retention time.
Dental Caries:
The oral microbiota functions as a part of the host defense by acting as a barrier,
e.g., by competition for essential nutrients and creation of unfavorable conditions to
exogenous organisms that may be pathogenic to the host. Over 700 bacterial taxa have
been found in the oral cavity, however they are not all present in the same mouth. The
composition varies in different sites in the oral cavity, with e.g., a large and more
diverse bacterial load on the dorsum of the tongue. Most of these microbes are
harmless, but under certain conditions some can cause oral infections like caries or
periodontal disease. Oral streptococci, like Streptococcus mutans, are associated with
pyogenic and other infections in various sites including mouth, heart, joints, skin,
muscle, and central nervous system.
The destruction of the enamel, dentin or cementum of teeth due to bacterial
activities. During the consumption of easily fermentable carbohydrates (sucrose)
stimulates the growth of oral microbes, most notably S. mutans. Due to the absence of
oxygen and the general fermentative metabolism on sucrose leads to the formation of
organic acids. Caries are initiated by direct demineralization of the enamel of teeth
due to lactic acid and other organic acids (pH < 5.0) which accumulate in dental
plaque (Figure 1). Lactic acid bacteria in the plaque produce lactic acid from the
fermentation of sugars and other carbohydrates in the diet of the host. Streptococcus
mutans and Streptococcus sobrinus have a central role in the etiology of dental caries
and has most consistently been associated with the initiation of dental caries, but other
lactic Lactobacilli are strong acid producers and hence cause an acidic environment
creating the risk for cavities. Usually, the appearance of S. mutans in the tooth cavities
is followed by caries after 6-24 months. These organisms normally colonize the teeth,
and this correlates with the incidence of decay on these surfaces.
Streptococcus mutans has a number of physiological and biochemical properties

which implicate it in the initiation of dental caries.
1. It is a regular component of the normal oral flora of humans which occurs in

relatively large numbers. It readily colonizes tooth surfaces: salivary components
(mucins, which are glycoproteins) form a thin film on the tooth called the enamel
pellicle.
2. It contains the enzyme glycosyl transferase that probably serves as the bacterial
ligand for attachment, and that polymerizes glucose obtained from dietary sucrose to
glucans which leads directly to the formation of plaque.
3.It produces lactic acid from the utilization of dietary carbohydrate which
demineralizes tooth enamel. S. mutans produces more lactic acid and is more acid-
tolerant than most other streptococci.
4. It stores polysaccharides made from dietary sugars which can be utilized as reserve
carbon and energy sources for production of lactic acid. The organisms can also form
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intracellular polysaccharides from sugars which are stored in cells and then
metabolized to lactic acid.
Figure 1: The ecological development of dental caries
Periodontal Diseases :
Are bacterial infections that affect the supporting structures of the teeth (gingiva,
cementum, periodontal membrane and alveolar bone). The most common form are:
1- Gingivitis: the earliest stage of periodontal disease is an inflammatory condition
of the gums. It is associated with accumulations of bacterial plaque in the area.
Increased populations of Actinomyces have been suggested as the causative agent.
This leads to swollen, bleeding gums, a sign of gingivitis (Table , Figure 3).
2- Gingival lesions: associated with specific bacterial infections in patients with and
without immunodeficiency. Neisseria gonorrhoeae, Treponema pallidum,
Mycobacterium chelonae, are the most common bacterial infections that give rise
to gingival lesions. They can manifest as fiery red, edematous, and painful
ulceration. Bacteria in these lesions are very complex populations consisting of
Gram-positive organisms (including Actinomyces and Streptococci) and Gram-
negative organisms (including Spirochetes and Bacteroides).
3- Periodontitis: Periodontal disease also can cause teeth loosing . This is a sign of
severe periodontitis (the advanced stage of disease). the mechanisms of tissue
destruction in periodontal disease are not clearly defined but hydrolytic enzymes,
endotoxins, and other toxic bacterial metabolites seem to be involved.
Capnocytophaga species are gram-negative, gliding anaerobes; Rothia species are
pleomorphic, aerobic, gram-positive rods. Both probably participate in the
complex microbial flora of periodontal disease with prominent bone destruction
(Table , Figure 3). Moreover, the most common viral infections are herpes
simplex virus (HSV-1), (HSV-2) and varicella-zoster virus. Candida albicans is a
diploid fungus (a form of yeast) that causes opportunistic oral and genital
infections in humans.
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Table 1: Frequency of common bacterial species in oral cavity
Bacterium Plaque Dental caries Gingivitis Periodontitis

Streptococcus sanguis ++ ++ ++ +
S. mutans ++ ++ 0 0
S. salivarius 0 0 0 0
Actinomyces viscosis + + ++ +
A. israelii + + ++ ++
Lactobacillus sp. + + 0 0
Propionibacterium acnes 0 + + ++
Bacteroides sp. 0 0 + ++
Selenomonas sputagena 0 0 + ++
Large Spirochetes 0 0 0 ++
++ = Frequently encountered in high proportions; + = Frequently encountered in low to

moderate proportions; 0 = Sometimes encountered in low proportions or not detectable.
Figure 2: Attachment of bacteria on tooth surface
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Figure 3: Developing of Periodontitis
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The Relation of Bacteria to Diseases
Mechanisms of Bacterial Pathogenicity
Microbial pathogenicity has been defined as the structural and biochemical
mechanisms whereby microorganisms cause disease. (e.g. capsules, fimbriae, LPS or
other cell wall components) or active secretion of substances that either damage host
tissues or protect the bacteria against host defenses.
Virulence : The ability of an agent of infection to produce disease or is a measure of
the severity of the disease it causes.
Pathogenesis: The term can also describe the origin and development of the
disease.
Infection: includes colonization, multiplication, invasion or persistence of a pathogen
on or within a host. There are two broad qualities of pathogenic bacteria underlie the
means by which they cause disease: invasiveness (ability to invade tissues) and
toxigenesis (ability to produce toxins).
Colonization: The first stage of microbial infection is colonization: the establishment
of the pathogen at the appropriate portal of entry
1- Mucus membrane of urogenital tract, the digestive tract, the respiratory tract
and the conjunctiva.
2- Skin through damaged tissue or by hair follicles and sweat glands
3- Parentarel: Microorganisms are deposited into the tissues below the skin
Types of Adherence to Cell or Tissue Surfaces
1. Nonspecific adherence: (reversible attachment) involves nonspecific attractive
forces are:
a. hydrophobic interactions : tendency of nonpolar substances to aggregate in aqueous
solution b. electrostatic attractions: is the phenomenon where a negatively charged
atom is attracted to a positively charged atom. c. Brownian movement: bacterial
swimming by randomizing direction. d. trapping by biofilm polymers.
2. Specific adherence: (permanent attachment) specific lock-and-key bonds between

complementary molecules on bacteria called adhesin and receptor (ligands) on hot
cell surface.
Invasion (invasiveness): Medical microbiologists have long referred to these

substances as invasions are proteins (enzymes) that act locally to damage host cells
and/or have the immediate effect of facilitating the growth and spread of the pathogen.
Bacterial Invasins
1-Spreading Factors is a descriptive term for a family of bacterial enzymes that affect
the physical properties of tissue matrices and intercellular spaces.
a) Hyaluronidase. is the original spreading factor It is produced by Streptococci,
Staphylococci and Clostridia. The enzyme attacks the interstitial cement "ground
substance" of connective tissue.
b) Collagenase is produced by Clostridium histolyticum and Clostridium perfringens.
It breaks down collagen, the framework of muscles, which facilitates gas gangrene due
to these organisms.
c) Neuraminidase is produced by intestinal pathogens such as Vibrio cholerae and
Shigella dysenteriae. It degrades neuraminic acid an intercellular cement of the
epithelial cells of the intestinal mucosa.
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d) Streptokinase and Staphylokinase are produced by Streptococci and
Staphylococci, respectively. Kinase enzymes convert inactive plasminogen to plasmin
which digests fibrin and prevents clotting of the blood.
2- Enzymes that Cause Hemolysis and/or Leucolysis
a) Phospholipases and Lecithinases produced by Clostridium perfringens (alpha
toxin), hydrolyze phospholipids in cell membranes or destroy lecithin
(phosphatidylcholine).
b) Hemolysins, notably produced by Staphylococci (alpha toxin), Streptococci
(streptolysin) and clostridia, that destroy red blood cells and other cells by lysis.
c) Leukocidins: kills WBC’s which prevents phagocytosis cause more tissue damage.
3- Staphylococcal coagulase
Coagulase, formed by Staphylococcus aureus, is a cell-associated and diffusible
enzyme that converts fibrinogen to fibrin which causes clotting.
4-Extracellular Digestive Enzymes : Heterotrophic bacteria, in general, produce a
wide variety of extracellular enzymes including proteases, lipases, glycohydrolases,
nucleases, etc.,
Toxins (Toxigenesis)
Poisonous substances produced by microorganisms as a primary pathogenicity factor,
in case of toxins present in the bloodstream called (Toxemia).
Types of toxins:
1-Exotoxins : proteins that carry out specific reactions are usually heat labile, soluble
in body fluids and rapidly transported throughout body in blood or lymph, mostly
secreted outside of the Gram positive bacterial cells. Toxins that have been altered
by heat or chemicals to form (Toxoid) and used as vaccines for diphtheria and tetanus.
a) Neurotoxins : that interfere with normal nerves impulses like in; Botulism caused
by Clostridium botulinum produce toxin works at the neuromuscular junction resulting
in muscle paralysis and Tetanus caused by Clostridium tetani produce neurotoxin acts
on nerves, resulting in the inhibition of muscle relaxation and tetanospasmin “spasms
or Lock Jaw”
b) Enterotoxins: effect cells lining of the G.I. tract ex. Cholera toxin leads to
electrolyte imbalance and H2O Loss (Diarrhea).
c) Staphylococcal Enterotoxin: Staphylococcus aureus produces an enterotoxin
similar to cholera toxin.
2-Endotoxins : part of the outer cell wall of Gram negative bacteria; Lipid A toxin is
a portion of the LPS responsible for fever that is associated with many Gram negative
bacterial infections. Endotoxins are heat stable and do not promote the formation of
effective antibodies and organisms that produce endotoxins include: Salmonella typhi
, Proteus spp., Pseudomonas spp. and Neisseria spp.
References:
1- Kayser, F.H., Medical Microbiology ( 2005).
2- Todar, Medical Micro. Online text book.
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University of Kufa Microbiology/Immunology
College of Dentistry 3rd Class, 2019-2020
Immunology
The central science that study of the molecular and cellular components that
comprise the immune system, including their function and interaction. Immunity is a
state of having sufficient biological defenses to avoid infection, disease, or other
unwanted biological invasion and toxins. Moreover, the response of the body’s
defense mechanism to recognize self and non-self and store it as ‘immunological
memory’ is related to the functions of the immune system of the body.
The immune system is divided into a more primitive innate immune system, and
acquired or adaptive immune system.
Innate or Non-Specific Immunity: Provide immediate defense (within minutes)

against infection, and are found in all classes of plant and animal life. Innate
immunity is the first line of natural defense in the body and has broad specificity.
Function of innate immunity: non-specific defense mechanisms are very diverse.

Broadly they include:
1- Physical barriers (Anatomical barriers) to invasion, e.g. skin and mucous
membranes; effects of body temperature; mechanical reflexes such as coughing
and sneezing and watering of the eyes.
2- Chemical effects of substances (Physiological barriers) such as gastric acid,
oxygen and lysozyme.
3- Biological barrier, eg. Normal bacterial flora
4- Recruiting immune cells to sites of infection and inflammation through the
production chemical factors, called cytokines.
5- Activation of the complement cascade to identify bacteria and to promote
clearance of dead cells or antibody complexes.
6- The identification and removal of foreign substances in organs, tissue, blood and
lymph, by specialized white blood cells.
7- Activation of the adaptive immune system through a process known as antigen
presentation.
Cells of the innate immune system
 Natural Killer (NK) cells :Identify and kill virus-infected and tumour cells
and Complex recognition system- recognize MHC molecule.
 Macrophages : Mononuclear phagocytes for garbage disposal and present
foreign cells to immune system
 Granulocytes: include :
Neutrophils: Phagocytic Poluymorphonuclear Neutrophils (PMN): multi-lobed
nucleus. 50-70% of circulating WBC. Eosinophils: Bi-lobed nucleus 1-3% of
circulating WBC. Required for immune response to parasites, helminths and allergic.
Basophils: Not phagocytic- release granules containing histamines, serotonin,
prostaglandins. Represent <1% of circulating WBC (Fig 1).
Adaptive or Specific Immunity (Acquired)

The adaptive immune system is composed of highly specialized, systemic cells and
processes that eliminate pathogenic challenges. The adaptive immune response
provides immune system with the ability to recognize and remember specific
pathogens.
Active immunity: which develops throughout our lives and involves the lymphocytes
and develops in people are exposed to diseases or immunized against diseases through
vaccination.
Passive immunity : is "borrowed" from another source and it lasts for a short time.
For example, antibodies in a mother's breast milk provide a baby with temporary
immunity to diseases of the mother has been exposed.
Functions of adaptive immunity Adaptive immunity is triggered when a pathogen

evades the innate immune system , these include:
1. The recognition of specific “non-self” antigens in the presence of “self”, during the
process of antigen presentation (Fig 2).
2. The development of immunological memory, in which each pathogen is
“remembered” by a signature antigen. (Fig 2).
Cells of the acquired immune system
Lymphocytes : A granular leukocytes . 20-40% of the circulating WBC , 99% of the cells in
lymphatic circulation includes (Fig 1):-
1- T (thymus-derived) cells
 Helper T cells: recognize antigen, help B cells to make antibodies and Cytotoxic T cells
for killing.
 Cytotoxic T cells: poisonous to cells, kill cells infected by viruses and intracellular
bacteria
2- B (bone marrow-derived) cells
 Make antibodies
 Have insoluble antigen-binding receptor on its surface.
Figure 1: All the immune cells

Antigens: are glycoprotein molecules which react with antibodies or T cells.
However not all antigens can induce an immune response in the host: those that can
are termed Immunogens: means any agent which generates immune response. All
immunogens are antigens but not all antigens are immunogens. The ability of a
substance to induce immune response is referred to as immunogenicity which depend
on : Route of entry of immunogen into the host , Foreingnness, Molecular size, Dose
of immunogen and chemical composition.
Hapten: Small foreign molecule that is not antigenic. Must be coupled to a carrier
molecule to be antigenic.
Adjuvant: The substances, which enhances the immune response to immunogen are
called adjuvant. Adjuvants may be added to a vaccine to modify the immune response
by boosting it such as to give a longer-lasting protection. eg. A water-oil emulsion
used in BCG (Bacillus Calmette–Guérin) vaccine for tuberculosis.
Types of Antigens: Most are proteins or large polysaccharides:

1-Infectious materials: Capsules, cell walls, toxins, viral capsids, flagella, etc.
2- Non infectious materials:
a. Allergens materials like; dust, pollen, hair, foods, bee venom, drugs, and other
agents causing allergic reactions.
b. Foreign tissues and cells (from transplants and transfusions).
c. the body's own cells that the body fails to recognize as "normal self" (cancer cells,
infected cells, cells involved in autoimmune diseases)..
The body recognizes antigens by the three-dimensional shapes or regions called

antigenic determinants or epitopes. Antigenic determinants may be mutivalent, or
monovalent. Mutivalent antigens elicit a stronger immune response than monovalent
antigens. Multivalent antigen, variously called hetrologus antigen, can react with
antibodies produced in response to different antigen .
Figure 2: Stages of specific immune response

Humoral Immunity
Humoral immunity is called as such, because

it involves substances found in the humours, or
body fluids. It is the aspect of immunity that is
mediated by secreted antibodies, produced in the
cells of the B lymphocyte. Once a B cell
encounters its specific antigen and receives
additional signals from a T helper cell, it further
differentiates into an effectors cell, known as a
plasma cell (Fig 3). Plasma cells are short lived
cells (2-3 days) which secrete antibodies. These
antibodies bind to antigens, making them easier
targets for phagocytes, and trigger the
complement cascade. About 10% of plasma
cells will survive to become long-lived antigen
specific memory B cells.
Figure 3: Role of B cell in humoral immunity
Functions of humoral immunity

1- Identifying and neutralizing foreign objects like bacteria and viruses.
2- It can cause agglutination and precipitation of antibody-antigen products, and
stimulate other immune responses by phagocytosis, and the complement pathway.
3- If an incompatible blood transfusion has been done, causes a transfusion reaction,
which is mediated by the humoral immune response. This type of reaction, called an
acute hemolytic reaction, results in the rapid destruction (hemolysis) of the donor red
blood cells by host antibodies.
Cell Mediated Immunity
Cell-mediated immunity is an immune response that does not involve antibodies but
rather involves the activation of macrophages, natural killer cells (NK), antigen-
specific cytotoxic T-lymphocytes, and the release of various cytokines in response to
an antigen. T cells play a central role in cell-mediated immunity. It is most effective
in removing virus-infected cells, but also participates in defending against fungi,
protozoans, cancers, and intracellular bacteria. It also plays a major role in transplant
rejection.
Helper T cells (TH cells): secrete small proteins called cytokines that regulate or
"help" the immune response. they express the CD4 glycoprotein at their surface
Cytotoxic T cells (TC cells) destroy virally infected cells and tumor cells, and are also
implicated in transplant rejection. they express the CD8 glycoprotein at their surface
Memory T cells are a subset of antigen-specific T cells that persist long-term after an
infection has resolved.
Regulatory T cells (Treg cells), formerly known as suppressor T cells, are crucial for
the maintenance of immunological tolerance.
Functions of cellular immunity
1. activating antigen-specific cytotoxic T-lymphocytes that are able to induce apoptosis in

body cells, such as virus-infected cells, cells with intracellular bacteria, and cancer cells.
2. activating macrophages and natural killer cells, enabling them to destroy intracellular
pathogens.
3. stimulating cells to secrete a variety of cytokines that influence the function of other
cells involved in adaptive and innate immune responses.
Complement
The ability of specific proteins in the serum to cause lysis of bacteria and described
by:
• major role in innate and antibody-mediated immunity .
• complex series of ~30 proteins and glycoproteins (C1-C9 and A,D,P factors also
Mannan-binding-lactin(MBL)), total serum conc. 3-4 mg/ml.
• triggered enzyme cascade system; initially inactive precursor enzymes, and as a few
enzymes are activated, they catalyse the cleaving of secondary components etc.
• rapid, highly amplified response and very sensitive.
• components produced mainly in the liver and take different pathways include:
1- The Classical Pathway : initiated by antigen-antibody complexes
2- The Alternative Pathway : direct activation by pathogen surfaces
3- The Lectin Pathway : antibody-independent activation of classical pathway by
lectins which bind to carbohydrates only found on pathogens.
• Ends with the formation of the Membrane Attack Complex (MAC) . As a bi-product
of the classical pathway, fragments cleaved are pro-inflammatory molecules
Function
1. Cytolysis: by Membrane Attack Complex
2. Opsonisation : Phagocyte recognize the C3b antigen binding complex
3. Inflammation/chemotaxis: C5a, as chemotactic factors for neutrophils
Immunoglobulins
Glycoprotein molecules that are produced by plasma cells in response to an
immunogen and which function as antibodies.
Antibody: Structure
Antibodies are glycoprotein and are antigen-specific they produced by B-cell and
bind and inactivate foreign particles . Each antibody consists of four polypeptides -
two heavy chains and two light chains connected by disulfide bonds, joined to form a
"Y" shaped molecule.
Heavy Chain Each heavy chain has two regions, the constant region and the variable
region .
•Light Chain A light chain has two domains one constant domain and one variable
domain . Each antibody contains two light chains that are always identical. Some
parts of an antibody have unique functions. The tips of the Y contain the site that bind
antigen and, therefore. This region of the antibody is called the Fab (fragment,
antigen binding). The base of the Y plays a role in modulating immune cell activity.
This region is called the Fc (Fragment, crystallizable) region, and is composed of
two heavy chains.
In the course of B-cell maturation, IgD, IgM, are membrane bound antibodies and
instead IgG, IgE, or IgA which are secreted by the cell. The mechanism that causes
the production of antibodies to change from IgM or IgD to the other antibody
isotypes, IgE, IgA, or IgG, that have defined roles in the immune system is called
heavy chain class switching or isotype switching .
Antibody Functions
Antibodies contribute to immunity in three ways:
1–they prevent pathogens from entering or damaging cells by binding to them.
2–they stimulate removal of pathogens by macrophages and other cells by coating the
pathogen.
3–they trigger destruction of pathogens by stimulating
other immune responses such as the complement
pathway.
Mechanisms of Antibody Action

•Precipitation of soluble antigens
•Agglutination of foreign cells
•Neutralization
•Enhanced phagocytosis
•Complement activation leading to cell lysis
•Stimulates inflammation
Monoclonal antibodies means antibody that reacts with single type of antigen and
can have
College of Dentistry 3 rd Class, 2019-2020
Immune Response
The primary immune response occurs when an antigen comes in contact to the
immune system for the first time. During this time the immune system has to learn to
recognize antigen and how to make antibody against it and eventually produce
memory lymphocytes. The secondary immune response occurs when the second time
(3rd, 4th, etc.) the person is exposed to the same antigen. At this point immunological
memory has been established and the immune system, the main differences in the
following :
Table 1: Differences between Primary and Secondary Immune Response
Primary vs Secondary Immune Response
Primary Immune Response is the reaction Secondary Immune Response is the reaction
of the immune system when it contacts an of the immune system when it contacts an
antigen for the first time. antigen for the second and subsequent times.
Responding Cells
B cells and T cells are the responding Memory cells are the responding cells of the
cells of the primary immune response. secondary immune response.
Time Taken to Establish Immunity
Primary immune response takes a longer Secondary immune response takes a shorter
time to establish immunity. time to establish immunity.
Amount of Antibody Production
Generally, low amounts of antibodies are Generally, high amounts of antibodies are
produced during the primary immune produced during the secondary immune
response. response.
Type of Antibodies
IgM antibodies are mainly produced IgG antibodies are mainly produced during
during this immune response. A small this immune response. Small amounts of IgM
amount of IgG is also produced. are also produced.
Antibody Affinity for Antigen
Affinity of the antibodies towards Affinity of the antibodies towards antigens is
antigens is less. high.
Antibody Level
Antibody level declines rapidly during Antibody level remains high for a longer
primary immune response. period during the secondary immune
response.
Location
Primary immune response appears Secondary immune response appears mainly
mainly in lymph nodes and spleen. in bone marrows, then in lymphs and spleen.
Strength of the Response
Primary immune response is usually Secondary immune response is stronger.
weaker than secondary immune response.
Major histocompatibility antigens (MHC)

The human leukocyte antigen (HLA) system is a gene complex encoding the major
histocompatibility complex (MHC) proteins in humans. MHC antigens as cell-surface
proteins (also called transplantation antigens) mediate rejection of grafts between two
genetically different individuals. HLA (human leukocyte antigens) are the MHC
antigens of humans, and called so because they were first detected on leukocytes.
HLA genes are highly polymorphic, which means that they have many
different alleles, allowing them to fine-tune the adaptive immune system. The
essential role of the MHC antigens lies in the induction and regulation of the immune
response and defense against microorganisms. The physiologic function of MHC
molecules is the presentation of peptide antigen to T lymphocytes. These antigens and
their genes can be divided
into three major classes: class
I, class II and class III.
Antigen Presenting Cell

The process of displaying
antigen by MHC molecules is
called antigen presentation.
Specialized cells displaying
antigen as class II MHC
molecules are referred to as
antigen presenting cells
(APCs), even though all
nucleated cells express MHC
class I molecules and can
present antigen via these
molecules.
The major professionals APCs

1- Mononuclear Phagocytes (macrophages): when localized in tissues are
referred to as macrophages e.g. macrophages lining the sinusoids of the liver
are known as Kupffer cells in the skin named Langerhans’ cells and those
found in the brain are microglial cells.
2- Dendritic Cells : Follicular dendritic cells are found in B lymphocyte areas of
lymph nodes and spleen. These cells present antigen to B lymphocytes.
3- B Lymphocytes: are also rich in surface class II molecules and have been
shown to process and present antigen.
.
MHC Class I Antigen
MHC class I molecules are found on the cell surface of all nucleated cells in the body
Antigenic peptides that bind to MHC class I molecules are typically derived from
viral proteins (foreign antigens) to display for cytotoxic T cells (Figure 1). These
viral proteins are degraded by the host cell's proteasomes into small peptide
fragments. Peptides generated in the cytoplasm are transported into the endoplasmic
reticulum Newly synthesized MHC class I molecules assemble in the endoplasmic
reticulum, and the peptides bind to the MHC molecule, the peptide-MHC complex
leaves the endoplasmic reticulum and is transported through the Golgi apparatus to
the cell surface.
Figure 1. Model of MHC Class I antigen presenting pathway

MHC Class II Antigen Processing
MHC class II associated peptides are derived from antigens captured and
internalized by all cell types, but normally occurs only on professional antigen-
presenting cells (APCs): macrophages, B cells, and especially dendritic cells (DCs).
These antigens are degraded enzymatically, in endosomes and lysosomes, into
peptides that bind MHC class II molecules (Figure 2). Class II MHC molecules are
synthesized in the endoplasmic reticulum and are transported to endosomes . Once
such endosomes fuse with a vesicle containing foreign antigen, which then places
foreign peptides in the groove of the MHC class II molecule. The peptide MHC
complex then transits to the cell surface .
Figure 2. Model of MHC Class II antigen presenting pathways.

MHC restriction and T lymphocytes activation

The interaction between T lymphocytes and antigen and the class II molecule is
highly specific and will result in specific T cell proliferation and differentiation.
These lymphocytes are said to be genetically restricted by the class II molecule on
which the antigenic determinants was first recognized. This is called MHC restriction.
CD4+ T lymphocytes can either mediate macrophage activation or act B cells in
antibody responses by secreting cytokines. cytotoxic T lymphocytes (CTLs)
expresses CD8 receptors. When a CTL's CD8 receptor docks to a MHC class I
molecule and fits the epitope within the MHC class I molecule, the CTL triggers the
cell to undergo programmed cell death by apoptosis (killer T cells)
Lymphokines :
Lymphokines are a subset of cytokines that are produced by a type of immune
cell known as a lymphocyte. They are protein mediators typically produced by T
cells to direct the immune system response by signaling between its cells.
Lymphokines have many roles, including the attraction of other immune cells,
including macrophages and other lymphocytes, to an infected site and their
subsequent activation to prepare them to mount an immune response. Important
lymphokines secreted by the T helper cell include: Interleukin 2,3,4,5 and 6
Granulocyte-macrophage colony-stimulating factor and Interferon-gamma.
Figure 3. Overview of cellular interactions of the immune response and lymphocytes activation.
Immunity of the oral cavity
The oral cavity is a unique anatomical structure, characterized by the
juxtaposition of soft and hard tissues and which is continuously subject to challenge
by the external environment and foreign material. Diseases and disorders caused by
oral microorganisms are very common and economically important, in
particular dental caries and periodontitis (‘gum disease’; chronic destructive
inflammation of the supporting tissues of the teeth caused by anaerobic bacteria).
Also, halitosis (oral malodour) is caused by sulphide- producing oral bacteria. Oral
diseases secondary to systemic disease, e.g. oral candidiasis, due to acquired
immunodeficiency are of increasing clinical importance. Also, several autoimmune
diseases such as Sjögren’s syndrome and pemphigus vulgaris have oral
manifestations. Hence, an effective defence mechanism is necessary within the oral
cavity to safeguard it from these attacks. These defence mechanisms can be broadly
divided into:
1. Integrity of oral mucosa and role of lymphoid system.

This mucosa provided remains intact, few microorganisms can penetrate the
underlying tissues. This partly reflects the functions of the Keratin barrier and
Basement membrane. The oral cavity is lined by a stratified squamous epithelium
whose functions include:
1-Forming a primary structure barrier between the internal and external environment.
2- Protection against mechanical damage.
In the lamina propia adjacent to the basement membrane as apart of MALT there are a
few lymphoid cells which may combat microorganisms that penetrate to this depth.
These intraoral lymphoid aggregations, function together with the extra oral lymph
nodes for the protection of the oral cavity as a whole. There are in fact several intra
oral lymphosis aggregations.
1. The palatine tonsils comprise paired lymphoid masses, between the glossopalatine
and pharyngo palatine arches. The component lymphoid tissue contains both B and T
cells.
2. The lingual Tonsils are much less prominent lying on each side of the tongue just
distal to the circum vallate papillae. They contain lymphoid modules some of which
have germinal centers in addition to perifellicular diffuse lymphoid cells.
3. The pharyngeal tonsil comparison of simple mass of lymphoid tissue under the
nasopharangeal mucosa.
2. Role of Gingival crevicular fluid
With continued plaque accumulation at the cervical surface of the tooth, This fluid
contains immunoglobulins IgG, A, M in adition to complement components namely
C3, C4 and C5 and C3 Pro activator. Thus the crevicular fluid contains most of the
humoral and cellular immune components found in the blood, altering salivary IgA is
the predominant component. There are a number of other components of the
crevicular fluids including: Albumin, lysosomal enzymes, Transferring lysozyme,
traptaglobulin, Tryaluronidase, Glycoproteins, Collagenase, Lipoproteins but also
also contains macrophages, T and B cells which migrate from the underlying blood
vessels.
3. Role of saliva
In addition to mechanical lavage the saliva function as a component of the oral
immune system saliva combines both specific and non specific immune components.
1) NON SPECIFIC COMPONENTS include:
a. Lysozyme (Meramidase) This is bactericidal enzyme that splits the bond between
N acetyl glucosomine and N acetyl inuramic acid in the micopeptide components of
bacterial cell wall. Apart from S. mutans, the oral flora is generally resistant to
lysozyme.
b. Peroxidase thiocyanate ions and hydrogen peroxide, peroxidase kills acidophilus
by inhibiting lysin uptake and may inhibit some streptococci by limiting the action of
their glycolytic enzymes.
c. Lactoferrin This has a bacteriostatic effect on a whole microbial spectrum,
possibly by depleting local environmental iron required for microbial growth.
2) SPECIFIC COMPONENTS
a. Secretory IgA: IgA is quantitatively the most important Ig present in saliva,
mainly derived locally from plasma cells. It is then trasported and exerted into the oral
cavity secretor IgA also appears to limit microbial adherence to the mucosal surface.
b. Secretory immune system: this system comprises mucosal associated lymphoid
tissues eg. Local Ig A containing tissue and peyer’s patches.
c. Neutrophil-antibody-complement system comprises phagocytic blood and tissue
PMNs Leucocytes They serve as a powerful host reference mechanism to combat the
colonization and invasion by oral microbial flora. The PMNs do met work in isolation
but in concert with IgG and IgM antibodies and complement. The Ig G antibody coats
the microorganism then binds to PMNs surface receptors for the Fc portion of the Ig
G to enhance phagocytosis. by the PMN, it can be killed by:
1. oxidative mechanism these involve reactive oxygen specie like, H2O2.
2. non oxidative mechanism These important mechanisms result from PMN derived
lysozyme, lactoferrin and cathepsins which kill microorganisms directly in the
absence of O2 under anaerobic conditions.
d. Lymphocyte, macrophage and lymphokine mainly comprises effector T
lymphocytes, whose function include the following:
1. T- helper and T- suppressor lymphocytes regulate T effector cell activity and
antibody production by B lymphocytes.
2. T lymphocyte modulations of macrophage activity.
3. Specific lymphocyte stimulation by antigens which results in lymphokine

production which includes - Osteoblast activating factor (OAF) - Lymphotoxin (LT) -
Macrophage activation factor (MAF) Migration inhibition factor (MIF) - Lymphocyte
inhibitory factor (LIF) .
Immunity of Periodontal Disease

The effect of dental plaque on the immune response are both complex and varied.
It results:
1. In the activation of complement pathways.
2. Lymphocytic stimulation
3. Lymphokine release
4. Macrophages activation
The potent reactions are probably modulated by effects of the dental plaque
components resulting primarily in a localized chronic inflammatory response in the
gingiva. Unless meticulous oral hygiene is maintained chronic periodontic diseases.
For ease, it has been subdivided into four stages. Each stage in associated with certain
immune treatment.
1. In the initial lesion, there is a localized inflammatory reaction at the gingival
sulcus. This correlates with a localized inflammatory response of PMLs reflecting
chemotactic action of plaque antigen and complement activation.
2. The subsequent early lesion involves the local gingival tissue infiltration of
predominantly T cells and a few B- cells. In the circulation, lymphocytes are
sensitized as shown by their ability to release lymphokines.
3. In the established lesion, there is a characteristic localized plasma cell infiltration of
the gingival tissues.
4. The advanced lesion marks the transition to an advanced irreversible destructive
process readily and alveolar bone loss.
Hypersensitivity
Refers to undesirable (damaging, discomfort producing and sometimes fatal)
reactions produced by the normal immune system. including allergies . They are
usually referred to as an over- reaction of the immune system. Hypersensitivity
reactions require a pre-sensitized (immune) state of the host. Hypersensitivity
reactions can be divided into four types: type I, type II, type III and type IV, based on
the mechanisms involved and time taken for the reaction as following:
Autoimmunity
The immune system specifically recognizes and eliminates foreign agents thereby
protecting the host against infection. During maturation of the immune system,
immune cells that react against self-tissues are eliminated providing an immune
system that is „tolerant‟ to self.
Autoimmunity is defined as the development of immune system reactivity in the form
of auto-antibodies and T-cell responses to self-structures.
Autoimmune disease: This definition includes a variety of diseases which can be
described by the irregular functioning of the immune system that causes an
individual‟s immune system to generate antibodies which attack their own body
tissues.
For clinicians, autoimmune diseases appear to be either systemic (e.g. systemic lupus
erythematosus) or organ-specific (e.g. Type 1 diabetes mellitus). A combination of
genetic predisposition and environmental factors (infectious agents, chemicals, drugs
and vaccines ) contribute to the development of autoimmune disease
Cell mediated autoimmune diseases : Immune cells damage tissues directly by
killing cells or indirectly by releasing cytotoxic cytokines, prostaglandins, reactive
nitrogen or oxygen intermediates. Tissue macrophages and monocytes can act as
antigen-presenting cells to initiate an autoimmune response. Macrophages and
neutrophils damage tissues by releasing highly cytotoxic proteins like nitric oxide and
hydrogen peroxide..
Antibody-mediated autoimmune diseases Autoantibodies can induce damage to the
body by binding to self-tissues, activating the complement cascade and inducing lysis.
This occurs in certain forms of haemolytic anemia when autoantibodies bind to red
blood cell surface antigens inducing lysis of red blood cells .
Induction of Autoimmunity (Proposed mechanisms )
1- Sequestered antigens: Some self-antigens are sequestered (hidden) in
specialized tissues. These are not seen by the developing immune system will
not induce self-tolerance. Exposure of T cells to these normally
sequestered/tissue-specific self-antigens . Examples of Sequestered Antigens:
a) Myelin basic protein (MBP)
b) Sperm-associated antigens in some individuals following vasectomy
c) Lens and corneal proteins of the eye following infection or trauma
d) Heart muscle antigens following myocardial infarction
2- Molecular Mimicry (Cross-reacting Antigens): Viruses and bacteria
possess antigenic determinants that are very similar, or even identical, to
normal host cell components. This phenomenon, known as molecular
mimicry, occurs in a wide variety of organisms. Molecular mimicry may be
the initiating step in a variety of autoimmune diseases. As in
a) Human cytomegalovirus and HLA-D molecule
b) Papilloma virus and insulin receptor
c) Klebsiella pneumonia and HLA-B 27 molecule
3- Inappropriate Expression of Class II MHC Molecules: Class II MHC
ordinarily expressed on antigen presenting cells, such as macrophages,
dendritic cells and B cells. Abnormal expression of MHC determinants allows
the recognition of these auto-antigens by self-reactive T cells. Type I
Diabetes: Pancreatic β cells express abnormally high levels of MHC I and
MHC II.
4- Polyclonal B Cell Activation: Viruses and bacteria can induce nonspecific
polyclonal B cell activation. Polyclonal activation leads to the activation of
self-reactive B cells and autoantibody production. Patients with infectious
mononucleosis (caused by EBV) and AIDS (HIV) have a variety of auto-
antibodies.

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University of Kufa Microbiology

College of Dentistry 2019-2020 3rd Class

The Nature of Host-parasite Interactions in Humans

1. Mutualism: Both members of the association are benefit. This is a type of

(2) The transient flora (Exogenous microbiota) consists of nonpathogenic or

Normal Flora of the Human Oral Cavity.

Ecology of oral cavity

1-Temperature: Relatively constant 34˚-36 allows a large number of

2. REDOX Potential Eh: These processes depend on the oxygen during

7. Antimicrobial agents: Antibiotics suppress the resident microflora, leading

The oral flora and causes oral diseases

Abscesses, dental caries, gingivitis, and periodontal disease; If oral

Following are the primary beneficial effects of the normal flora.

2. Normal flora prevent colonization by pathogens by competing for

3. Normal flora may antagonize other bacteria through the production of

4. Normal flora stimulate the development of certain tissues, i.e., the

5. Normal flora stimulate the production of cross-reactive antibodies.

6. Normal flora achieved colonization resistance through the saturation of

Figure 1: Distribution of the microflora at distinct sites in the mouth.

DENTAL CARIES AND PERIODONTAL INFECTIONS

Role of Oral Streptococci in The Formation of Extracellular Polysaccharides

Streptococcus mutans has a number of physiological and biochemical properties

1. It is a regular component of the normal oral flora of humans which occurs in

Figure 1: The ecological development of dental caries

Bacterium Plaque Dental caries Gingivitis Periodontitis

++ = Frequently encountered in high proportions; + = Frequently encountered in low to

Figure 2: Attachment of bacteria on tooth surface

Figure 3: Developing of Periodontitis

2. Specific adherence: (permanent attachment) specific lock-and-key bonds between

Invasion (invasiveness): Medical microbiologists have long referred to these

Innate or Non-Specific Immunity: Provide immediate defense (within minutes)

Function of innate immunity: non-specific defense mechanisms are very diverse.

Adaptive or Specific Immunity (Acquired)

Functions of adaptive immunity Adaptive immunity is triggered when a pathogen

Figure 1: All the immune cells

Types of Antigens: Most are proteins or large polysaccharides:

The body recognizes antigens by the three-dimensional shapes or regions called

Figure 2: Stages of specific immune response

Humoral immunity is called as such, because

Figure 3: Role of B cell in humoral immunity

Functions of humoral immunity

1. activating antigen-specific cytotoxic T-lymphocytes that are able to induce apoptosis in

Mechanisms of Antibody Action

Primary vs Secondary Immune Response

Major histocompatibility antigens (MHC)

Antigen Presenting Cell

The major professionals APCs

Figure 1. Model of MHC Class I antigen presenting pathway

Figure 2. Model of MHC Class II antigen presenting pathways.

MHC restriction and T lymphocytes activation

1. Integrity of oral mucosa and role of lymphoid system.

3. Specific lymphocyte stimulation by antigens which results in lymphokine

Immunity of Periodontal Disease

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