Immunology & Serology Review Notes

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The key takeaways are the components of the innate and adaptive immune systems, as well as the functions of secondary lymphoid organs.

The components of the innate immune system include acute phase reactants, cellular defenses like phagocytes and natural killer cells, and soluble factors like complement proteins and defensins.

The components of the adaptive immune system include B cells and T cells. B cells produce antibodies and T cells mediate cell-mediated immunity.

IMMUNOLOGY & SEROLOGY

Source: Immunology and Serology Review 2016-2017 by Jude Anthony Trinidad, RMT, MSMT, MLS(ASCPi)
Immunology
Study of our immune system; Study of hosts reaction when foreign antigens are introduced to the body
HISTORY
1978 Edward Jenner Vaccination (smallpox) cowpox
1868 Louise Pateur Founder of Immunology
1880-1800 Elli Methnikof Cellular Theory of Immunity
1901 Bordet and Gengou Complement Fixation
1952-1953 Grabar and Williams Immunoelectrophoresis Analysis in Gels
1896 Erhlich Side Chain Theory
1930 Friedrich Brent/Felix Haurowitz Template Theory of Antibody Production
1955-1957 Niels K. Jerne/Frank Burnet Clonal Selection theory
1958 Dausset/Rapaport Histocompatibility complex
1973 Milstein/Kohler Hybridoma for the production of Monoclonal Antibodies
Categories/Components of the Immune system
NATURAL IMMUNITY Innate; non-specific-- ADAPTIVE IMMUNITY Acquired; specific (e.g.
targets all antibodies)
Ability of an individual to resist infection by Specificity foe each individual pathogen
means of normally present body functions Ability to remember a prior exposure
No prior exposure required Results in an increased response upon repeated
Response does not change with subsequent exposure (has memory)
exposures (lacks memory) Cells under adaptice: Lymphocytes
Cells under natural: Phagocytes eating e.g. B-cell (bone marrow)
organisms w/ digestive enzymes T-cell (thymus)
e.g. N, Mono, Macro
Natural Immunity
EXTERNAL DEFENSE SYSTEM INTERNAL DEFENSE SYSTEM
PREVENTS ENTRY OF INVADING RECOGNIZES THE INVADING PATHOGEN
PATHOGENS
Physical Cellular
Skin, mucous membrane Phagocyte
Cilia lining in respiratory tract Natural Killer cells (Kiss or death)
Biochemical Humoral (Soluble factors)
Lactic acid in sweat Acute phase reactants
Lysozymes Interferons (A&B)
Acidity of GIT and vagina Defensins
Normal Flora Complement proteins
*Hansels stain stain for Eosinophils
PART I. INNATE IMMUNITY
A. Acute Phase Reactants
Plasma proteins that increases rapidly by at least 25% due to infection, trauma or injury (produced primarily by
hepatocytes)
Response time
Protein Increase Functions
C-reactive protein 6-10 1000x Opsonization, complement activation
Seum amyloid A 24 1000x Removal of cholesterol
Alpha 1 antitrypsin 24 2-5x Protease inhibitor
Fibrinogen 24 2-5x Clot formation
Haptoglobin 24 2-10x Binds hemoglobin
Ceruloplasmin 48-72 2x Binds copper and oxidizes iron (e.g. wilsons
dse)
Complement C3 48-72 2x Opsonization, lysis
Source: Stevens, 2010
B. Cellular Defense Mechanisms
Myeloid line Monocytes
Neutrophils Dendritic cells (best; presenting
Basophils cells)
Eosinophils
C. Toll-like Receptors Phagocytes - TLR binds phagocytosis will occur
Highest concentration on: Examples
Monocytes TLR2 gram+bacteria
Macrophages TLR4 gram- bacteria
Neutrophils

D. Phagocytosis
Kills extracellular organisms; First described by Metchmikof
Steps:
Initiation Stage - surface receptors that allows for adherence
Chemotaxis - Migration of neutrophils and monocytes to the site of injury
- Chemotoxin E3 C3a C5a acts as signal
- 2 types of Chemotaxin: Positive and Negative
Engulfment - enclosing the pathogen into a phagocytic vacuole phagolysosome
- opson-make organism more susceptible to organism
Digestion and Excretion
Summary:
1. Chemotaxis and adherence of microbe to phagocyte
2. Ingestion of microbe by phagocyte
3. Formation of a phagosome
4. phagosome + lysosome = Phagolysosome
5. Digestion of ingested microbe by enzymes
6. Formation of residual body containing indigestible material
7. Discharge of waste materials.
HOW MICROORGANISMS ARE DESTROYED
Activation of NADPH oxidase
Nitric Oxide
Disease associated to Phagocytosis
Chronic Granulomatous dse
Afects neutrophil microbicidal action
Impaired NADPH production
Test: Nitro Blue Tetrazolium test (+) Colorless (N) Blue precipitate
Lazy Leukocyte Syndrome
Jobs Syndrome normal random movement
E. Inflammation
Rxn to tse injury
Cardinal signs:
Rubor - Redness ( bloodflow)
Calor - Heat (Interleukin 1 production) e.g. Dracula Medenisis
Dolor - Pain (WBC) lactic acid formation; Pyrugenia sensation;
Tumor - Swelling (release of plasma fluid in surrounding tse.)
Function laesa - Loss of fxn
Stages:
Vascular response - most cells release histamine- vasoconstriction; basophils
Cellular response
Resolution & Repair

PART II. ACQUIRED/ADAPTIVE/SPECIFIC IMMUNITY


A. TYPES
1. Naturally Acquired (Antigen) Long-term (response time is slow)
a. Active includes the type of immunity that develops during convalescence from an infection
b. Passive develops after the placental passage of antibody from mother to fetus
2. Artificially Acquired (Anti-body) Immediate (short term 3-6 mos.)
a. Active immunity from vaccination
b. Passive immunity obtained after injection f gamma globulin for the induction of immune state

Cells involve: lymphocytes


Marker: Terminal Deoxynucleotidul Transferase (TDT)
20-40% of circulation WBC
With large rounded nucleus, Nuclear Chromatin is dense
No granules
SURFACE IG - ANTIBODY FOUND IN THE SUFACE
T CELLS B CELLS
Cell Mediated immunity Humoral immunity (soluble)
Thymus Bone marrow
Lymphokines soluble factor produce Tcells Antibodies
60-80% 20-35%
Longer lifespan (4-10 yrs) Shorter lifespan (3-5 days)
Identified by erythrocyte-Rosette assay Surface immunoglobulin
B. LYMPHOID ORGANS site of diferentiation and maturation; growth of lymphocyte
A. Primary Lymphoid Organs: Bone marrow & Thymus
B. Secondary Lymphoid Organs drops the pathogens
a. Spleen - filtering antigens found in the blood (largest); main site of antibody production
b. Lymph nodes - filtering antigens found in tse fluid
c. Tonsils
d. Appendix
e. Peyers patches
f. Adenoid
Fxns of secondary lymphoid:
Trapping site of pathogens
Stand-by areas of T-cells, B- cells and Phagocytes
Place of encounter for pathogens and the cells
Production of antibodies, lymphokines; phagocytosis occurs
Antigenic dependent lymphopoesis
LOCATION
T CELLS B CELLS
Medullary, Perifolliculare and Paracortical Follicular and medullary (germinal center) of
regionof Lymph nodes lymph nodes
Periarteriolar Regions of spleen Primary follicles and red pulp of spleen
Thoracic duct of the circulatory system Follicular region of GALT

T LYMPHOCYTES
- 80% of the circulating lymphocytes in the peripheral blood
Subsets: T CELL RECEPTORS
T-helper cells (70% CD4+) Receptor of the HW CD2 sheep RBC receptor
T- suppressor cells (30% CD 8+) CD3 part of T cell antigen-receptor complex
T- cytotoxic cells C specific CD4 receptor of MHC class II molecule (Th)
T- delayed hypersensitivity CD8 receptor of MHC class I molecule (Ts & Tc);
Development major histocomplatibility
Double Negative Thymocytes (CD4- & CD8-)
Double positive thymocytes (CD4 & CD8+)
Mature T cell Single positive
Activated T cell Interleukin II (CD25) sensitized T-cell produce lymphokines
Memory T cell act as reserved/back-up
Sensitixed T cell
NATURAL KILLER CELL (NK)
- A.k.a. large granular lymphocyte (LGL); non-specific Virgin lymphocyte not yet exposed by the foreign antigen
- Kill infected and malignant cells
- Identified by presence of CD56& CD16, absence of CD3
- Activated by IL2 & IFN-gamma to become LAK cells
o LAK Lymphokine Activated Killer cells (specific)
Laboratory Identification of lymphocytes
Flow cytometry Cooled standard in identifying lymphocyte
Fluoresence Microscopy
Rosette assay
Density Gradient Centrifugation
o Ficoll-Hypaque - separate other lymphocyte fr other blood cells
o Roswell part Memorial Institute (RPMI) culture media of the
lymphocyte (4-10 yrs)
*1.077 gravity

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