CHAPTER 6

DISEASES OF THE IMMUNE SYSTEM

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THE NORMAL IMMUNE RESPONSE
!
INNATE IMMUNITY
• Defence mechanisms that are present even before infections that have evolved specifically
recognize microbes and protect individuals against infections
• Components:
• Epithelial barrier to block entry of microbes
• Phagocytic cells (neutrophils and macrophages)
• Dendritic cells
• Natural killer cells
• Plasma proteins
• Most important cellular reactions:
• Inflammation
• Anti-viral defence
!
ADAPTIVE IMMUNITY
• Mechanisms that are stimulated by microbes and are capable of recognizing microbial and non
microbial substances
• Two types:
1. Humoral → protects against extracellular microbes and their toxins
• Mediated by B lymphocytes and antibodies
2. Cell-mediated → defence against intracellular microbes
• Mediated by T lymphocytes
!!
COMPONENTS OF THE IMMUNE SYSTEM: CELLS, TISSUES, MOLECULES
Cells of the Immune System
T lymphocytes
• Develop from thymus
• 60-70% of lymphocytes
• Recognize specific cell-bound antigen using T-cell receptor
• The αβ TCR recognizes peptide antigens that are displayed by the major histocompatibility
complex (MHC) molecules on the surfaces of antigen presenting cells
• TCR diversity is generated by somatic rearrangement of the genes that encode the TCR α and
β chains
!
B lymphocytes
• Develop from bone marrow
• 10-20% of lymphocytes
• Recognize antigens via the B-cell antigen receptor complex composed of membrane bound
antibodies (IgM and IgD)
!
Dendritic cells
• 2 types
a) Interdigitating dendritic cells
 • Most important Ag presenting cells for initiating primary T cell responses against
protein antigens
• Located right under epithelia, a good place to capture antigens
• Immature dendritic cells w/in the epidermis are called Langerhans cells
• Express many receptors for capturing and responding to microbes
b) Follicular dendritic cells
• In germinal centres of lymphoid follicles
• Bear Fc receptors for IgG and C3b to trap antigens bound to antibodies or
complement
!
Macrophages
• Important in the induction and effector phases of adaptive immunity
• Function as APCs in T cell activation
• Eliminate intracellular microbes
• Participate in the effector phase of humoral immunity
!
Natural killer cells
• 10-15% of peripheral blood lymphocytes
• Do not express TCRs or Ig
• Larger than small lymphocytes and contain azurophilic granules
• Can kill a variety of infected and tumor cells without prior exposure or activation
• CD16 and CD56 on surface
• Antibody-dependent cell mediated cytotoxicity
• CD16 binds IgG allowing the NK cell to lyse IgG coated target cells
• The functional activity of NK cells is regulated by a balance between signals from
activating and inhibitory receptors
!
Tissues of the Immune System
Generative Lymphoid Organs
• T and B lymphocytes mature and become competent to respond to antigens
• Thymus – T cells
• Bone marrow – B cells
!
Peripheral Lymphoid Organs
• Lymph nodes
• Spleen
• Cutaneous and mucosal lymphoid systems
!
Lymphocyte Recirculation
• Lymphocytes constantly recirculate between tissues and home to particular sites, naïve
lymphocytes traverse the peripheral lymphoid organs where immune responses re
initiated, and effector lymphocytes migrate to sites of infection and inflammation
!
MHC molecules: Peptide Display System of Adaptive Immunity
Class I
• Expressed on all nucleated cells and platelets
• Encoded by HLA-A, HLA-B, HLA-C
• Display peptides that are derived from proteins such as viral antigens that are located in the
cytoplasm and usually produced in the cell
• Recognized by CD8+
!
Class II
• Encoded by HLA-D which has three regions
• DP
 • DQ
• DR
• Present antigens that are internalized into vesicles and are typically derived from
extracellular microbes and soluble proteins
!
HLA Associated Diseases
• Inflammatory diseases – ankylosing spondylitis (HLA-B27)
• Autoimmune diseases – autoimmune endocrinopathy (HLA-DR3/4)
• Inherited errors of metabolism – 21 hydroxylase deficiency (HLA-BW47)
!
Cytokines: Messenger Molecules of the Immune System
• Functional classes
• Cytokines of Innate Immunity
• Rapidly produced in response to microbes and stimuli
• Made by macrophages, dendritic cells, NK cells
• Mediate inflammation and anti-viral defence
• TNF IL-1, IL-12, type 1 IFN’s, IFN-γ, chemokines
• Cytokines of Adaptive Immunity
• Produced in response to antigen and other signals
• Made by CD4+ T lymphocytes
• Promote lymphocyte proliferation and differentiation, activate effector cells
• IL-2, IL-4, IL-5, IL-17, IFN-γ
• Colony-stimulating factors (stimulators of hematopoiesis)
!!
!
OVERVIEW OF LYMPHOCYTE ACTIVATION AND IMMUNE RESPONSES
!
The Display and Recognition of Antigens
• Clonal Selection Hypothesis - Lymphocytes specific for a large number of antigens exist before
exposure to the antigen, and when an antigen enters, it selects the specific cells and activates
them
!
Cell Mediated Immunity – Activation of T lymphocytes and Elimination of Intracellular Microbes
• Some of the progeny of the expanded T cells differentiate into effector cells that can secrete
different sets of cytokines, and thus perform different functions
• overall effector functions of CMI:
• macrophage activation - killing of ingested microbes
• inflammation
• killing of infected cells
!
Humoral Immunity – Activation of B lymphocytes and Elimination of Extracellular Microbes
• effector functions of of humoral immunity:
• Neutralization of microbes and toxins
• Opsonization and phagocytosis
• Antibody-dependent cytotoxicity
• Complement activation:
• Lysis of microbes
• Phagocytosis of opsonised microbes
• Inflammation
!
Decline of Immune Responses and Immunological Memory
• Effector cells die by apoptosis
 • Generation of long-lived memory cells

!!
HYPERSENSITIVITY AND AUTOIMMUNE DISORDERS
MECHANISMS OF HYPERSENSITIVITY REACTIONS
• Both exogenous and endogenous antigens may elicit hypersensitivity reactions
• Development of hypersensitivity diseases is often associated with the inheritance of particular
susceptibility genes
• Hypersensitivity reflects an imbalance between the effector mechanisms of immune responses
and the control mechanisms that serve to normally limit such response

Types of Hypersensitivity Reactions

Type of Reaction Prototypic Disorder Immune Mechanisms Pathologic Lesions
Immediate Anaphylaxis; allergies; bronchial Production of IgE antibody → Vascular dilation, edema, smooth
(type I) hypersensitivity asthma (atopic forms) immediate release of vasoactive muscle contraction, mucus
amines and other mediators from mast production, tissue injury,
cells; later recruitment of inflammatory inflammation
cells
Antibody-mediated Autoimmune hemolytic anemia; Production of IgG, IgM → binds to Phagocytosis and lysis of cells;
(type II) hypersensitivity Goodpasture syndrome antigen on target cell or tissue → inflammation; in some diseases,
phagocytosis or lysis of target cell by functional derangements without
activated complement or Fc receptors; cell or tissue injury
recruitment of leukocytes
Immune complex– Systemic lupus erythematosus; Deposition of antigen-antibody Inflammation, necrotizing
mediated some forms of complexes → complement activation vasculitis (fibrinoid necrosis)
(type III) hypersensitivity glomerulonephritis; serum → recruitment of leukocytes by
sickness; Arthus reaction complement products and Fc receptors
→ release of enzymes and other toxic
molecules
Cell-mediated (type IV) Contact dermatitis; multiple Activated T lymphocytes Perivascular cellular infiltrates;
hypersensitivity sclerosis; type I diabetes; 1. ease of cytokines → edema; granuloma formation; cell
rheumatoid arthritis; inflammation and destruction
inflammatory bowel disease; macrophage activation;
tuberculosis 2. T cell–mediated

!
AUTOIMMUNE DISEASES
Three requirements:
• Presence of an immune reaction specific for some self-antigen or self-tissue
• Evidence that such a reaction is not secondary to tissue damage but is of primary pathogenic
significance
• Absence of another well-defined cause of the disease
• Phenomenon of unresponsiveness to an antigen as a result of exposure of lymphocytes to that
antigen
!
Central tolerance:
• Immature self-reactive T and B lymphocyte clones that recognize self-antigens during their
maturation in the central lymphoid organs are killed or rendered harmless
• Negative selection
• Receptor editing
!
Peripheral tolerance:
• Anergy – prolonged, irreversible functional inactivation of lymphocytes induced by an
encounter with antigens under certain conditions
• Suppression by regulatory T cells
 • Deletion by activation induced cell death
• General Principles
• Progressive
• Sporadic relapses and remissions
• Damage becomes inexorable.
• Clinical and pathologic manifestations are determined by the nature of the
underlying immune response
• Different diseases have overlapping clinical, pathologic, and serologic features

!
SYSTEMIC LUPUS ERYTHEMATOSUS
• Multi-system autoimmune disease caused by antinuclear autoantibodies
• Characterized by injury to the skin, joints, kidney, and serosal membranes (“MD
SOAPBRAIN” for 11 criteria of SLE: need 4/11 for dx (serially or simultaneously))
• Kidney – lupus nephritis
• Skin – malar rash
• CNS – poorly defined symptoms
• Cardiovascular
• Pericarditis
• Endocarditis (Liebman-Sacks vegetations)
• Spleen – splenomegaly
• Lungs – Pleuritis and pleural effusions
• Bone Marrow – LE/hematoxylin bodies
!
SJOGREN SYNDROME
• Chronic disease characterized by dry eyes and dry mouth resulting from immunologically
mediated destruction of the lacrimal and salivary glands
• Autoantibodies to SS-A (Ro) and SS-B (La)
• Histology – periductal and perivascular lymphocytic infiltration in major and minor salivary
glands
• Biopsy of the lip is essential for the diagnosis of Sjorgren syndrome
• Lack of tears leads to drying of the corneal epithelium, which becomes inflamed, eroded, and
ulceration; and dryness and crusting of the nose may lead to ulcerations and even perforation of
the nasal septum
!
SYSTEMIC SCLEROSIS/SCLERODERMA
• Chronic disease characterized by:
• Chronic inflammation thought to be the result of autoimmunity
• Widespread damage to small blood vessels
• Progressive interstitial and perivascular fibrosis in the skin and multiple organs
• Diffuse
• Widespread skin involvement with rapid progression and early visceral involvement
• Limited
• CREST syndrome:
• Calcinosis
• Raynaud’s phenomenon
• Esophageal dysmotility
• Sclerodactyly
• Telangiectasia
• Cause unknown, tissue injury caused by autoimmune responses, vascular damage, and collagen
deposition
• Anti-Scl 70
• Histology – microvascular disease and progressive fibrosis
!
INFLAMMATORY MYOPATHIES
• Dermatomyositis
• Polymyositis
• Inclusion body myositis
• may show Jo-1 antibodies
!
MIXED CONNECTIVE TISSUE DISEASE
• Mixture of features between SLE, systemic sclerosis and polymyositis
• High titres of antibodies to ribonucleoprotein particle-containing U1 ribonucleoprotein
!
POLYARTERITIS NODOSA AND OTHER VASCULITIDES
!
REJECTION OF TISSUE TRANSPLANTS
Mechanisms:
!
1. Cell-mediated - “Cell mediated rejection”, a type of acute rejection
a. Direct Pathway
• Donor Class I and Class II MHC antigens on antigen presenting cells in the graft are
recognized by host CD8+ cytotoxic T cells and CD4+ helper T cells
• CD4+ cells proliferate and produce cytokines that induce tissue damage by a local
delayed hypersensitivity reaction
• CD8+ T cells responding to graft antigens differentiate into CTLs that kill graft cells
! b. Indirect Pathway
• Antigens are picked up and processed and displayed by host APCs and activate
CD4+ T cells, which damage the graft by a local delayed hypersensitivity reaction
and stimulate B lymphocytes to produce antibodies
!!
2. Antibody mediated
a. Hyperacute – preformed anti-donor antibodies are present in the circulation of the
recipient (within minutes to hours post transplant)
b. Acute – rejection vasculitis (can be within days or even months to years after), Cd4+
!
3. Chronic rejection
!
Graft vs. Host disease
• Occurs in any situation in which immunologically competent cells or their precursors are
transplanted into immunologically crippled recipients, and the transferred cells recognize
alloantigens in the host
• most commonly after bone marrow transplantation but can also occur in solid organ
• Acute or chronic
!!
IMMUNODEFICIENCY SYNDROMES
PRIMARY IMMUNODEFICIENCIES
!
X-linked Agammaglobulinemia
• Failure of B cell precursors to develop into mature B cells
• Mutated Bruton tyrosine kinase (Btk)
• Becomes apparent at 6 months of age, when maternal immunoglobulins are depleted
!
Common Variable Immunodeficiency
• Common but poorly defined entity with heterogeneity
 • Hypogammaglobulinemia
• Increased risk of lymphoid and gastric malignancy
!
Isolated IgA Deficiency
• Common (1/600), mostly whites
• Low levels of both serum and secretory IgA
• Basic defect is impaired differentiation of naïve B lymphocytes to IgA producing cells
!
Hyper-IgM Syndrome
• Make IgM but are deficient in the ability to produce IgG, IgA, and IgE antibodies
!
DiGeorge Syndrome (Thymic Hypoplasia)
• T-cell deficiency resulting from failure of development of the third and fourth pharyngeal
pouches
• Results from deletion of a gene on chromosome 22q11
• DiGeorge is a component of 22q11 deletion syndrome
!
Severe Combined Immunodeficiency (SCID)
• Defects in both humoral and cell-mediated immune responses
• Extremely susceptible to recurrent, severe infections of a wide range of pathogens
• Death within the first year of life without transplant
• Genetic defect in the X-linked form is a mutation in the common gamma chain subunit of
cytokine receptors – X-linked, 50-60%
• Deficiency of the enzyme adenosine deaminase – Autosomal Recessive
!
Wiskott-Aldrich Syndrome
• X-linked recessive disease characterized by thrombocytopenia, eczema, and marked
vulnerability to recurrent infection, ending in early death
• Mutation in WASP at Xp11.23
!
Genetic Deficiencies of the Complement System
!!
SECONDARY IMMUNODEFICIENCIES
• Cancer
• Diabetes
• Metabolic diseases
• Malnutrition
• Chronic infection
• Renal disease
• Chemotherapy
• Radiation
• Immunosuppressive therapy
!!
ACQUIRED IMMUNODEFICIENCY SYNDROME (AIDS)
!
• caused by retrovirus HIV; characterized by profound immunosuppression → opportunistic
infections, secondary neoplasms, and neurologic manifestations
• Five groups at risk
• Men who have sex with men
• IV drug users
• Hemophiliacs
 • Recipients of blood and blood components
• Heterosexual contacts of members of other high-risk groups
!
• Routes of Transmission
• Sexual transmission
• Parenteral transmission
• Mother to infant
• In utero by transplacental spread
• During delivery though an infected birth canal
• Breast milk
!
• Natural History - 3 main phases:
1. Primary infection, virus dissemination and Acute Retroviral syndrome (with host immune
response generated)
2. Middle, chronic phase (clinical latency)
3. Clinical AIDS (<200 CD4+ T-cells/µL)
!
Clinical Features in AIDS:
• AIDS defining Infections (opportunistic)
• Protozoal and Helminthic Infections
• Crytosporidiosis
• Toxoplasmosis
• Fungal Infections
• Pneumocystosis
• Candidiasis
• Cryptococosis
• Coccidioidomycosis
• Histoplasmosis
• Bacterial Infections
• Mycobacteriosis
• Nocardiosis
• Salmonella
• Viral Infections
• CMV
• HSV
• VZV
• Progressive multifocal leukoencephalopathy
!
2. Tumors
• Kaposi Sarcoma
• Lymphoma
• Systemic
• Primary CNS
• Body cavity
• Uterine cervix
• Anal carcinoma
!
3. CNS disease
• AIDS related dementia, encephalopathies, meningitis, etc.
!!
AMYLOIDOSIS
• Pathologic proteinaceous substance, deposited in the extracellular space in various organs and
tissue in a wide variety of clinical settings
• Amorphous, eosinophilic, hyaline, extracellular substance that, with progressive accumulation,
encroaches on and produces pressure atrophy of adjacent cells
• Continuous, non-branching fibrils, 7.5-10 nm diameter
• X-ray – cross-β-pleated sheet
!
• Not a chemically distinct entity – 3 major and several minor biochemical forms
• AL – Amyloid light chain, derived from Ig Light chains produced in plasma cells
• AA – amyloid associated, unique non-Ig protein synthesized by the liver in chronic
inflammatory states (eg. RA (most common), CTD’s, IBD, even assoc with malignancies such
as RCC, HL)
• Aβ - produced from β amyloid precursor protein and found in cerebral lesions of Alzheimer
disease
• Minor:
• Transthyretin (TTR) – senile systemic amyloidosis (normal TTR transport thyroxin and
retinoids, but mutated forms are not cleared)
• Aβ2 microglobulin – long term hemodialysis (the normal form of this protein is a normal
component of MHC class I molecules and in serum proteins)
• commonly manifests in synovium, joints and tendon sheaths in these pts
• Prion proteins
!
• Primary – associated with immunocyte disorder
• Plasma cell dyscrasia
• Secondary – as a complication of an underlying chronic inflammatory or tissue-destructive
process
• Chronic skin infections (skin popping)
• Hemodialysis-associated amyloidosis
• Hereditary or familial
• Familial Mediterranean fever
• Localized amyloidosis
• Endocrine amyloidosis
• Amyloid of aging
!
Another Classification:
1. Systemic (Generalized): such as AL, AA, Aβ2M
2. Hereditary: AA (Familial Mediterranean Fever) and ATTR (Familial Amyloidotic Myopathies)
3. Systemic Senile: ATTR (amyloid of aging)
4. Localized: Ab (Alzheimers), A Cal (in medullary thyroid ca), AIAPP (pancreatic islet amyloid),
AANF (isolated atrial amyloid)
!
Pathology
• Kidney – primarily glomerular deposition, looks like mesangial thickening
• Spleen – Two patterns:
• Sago – tapioca-like granules of follicular deposition
• Lardaceous – fusion of deposits into large, maplike areas
• Liver – primarily in the space of Disse
• Heart – enlarged, firm, deposits as focal subendocardial accumulations and within the
myocardium
• Other organs:
• Tongue
• Lungs
• Blood vessels
• Joints
Questions

1. What are the principal classes of lymphocytes and their functions in adaptive immunity
a. B lymphocytes – Plasma cell and antibody secretion
b. CD4+ helper cell – cytokine release, activation of macrophages, inflammation,
stimulation of B lymphocytes
c. CD8+ cytotoxic cell – kills cells infected with microbe

2.
!
List the three main categories of HLA associated diseases and give an example of each.
a. Inflammatory diseases – ankylosing spondylitis (HLA-B27)
b. Autoimmune diseases – autoimmune endocrinopathy (HLA-DR3/4)
c. Inherited errors of metabolism – 21 hydroxylase deficiency (HLA-BW47)

3.
!
List two mechanisms for determining monoclonality of lymphocytes:
a. TCR rearrangement – T cells
b. Ig gene rearrangement – B cells
! 4. What is Isolated IgA deficiency?
• Isolated IgA deficiency is a fairly common type of immunodeficiency. In the US, it
occurs in 1 in 600 people of European descent (but is less common in other ethnic
groups). As the name says, people with the disorder have a decreased amount of IgA
around - both in the serum and in secretions. The B cells in these patients have a hard
time differentiating into IgA-producing cells for some reason.
! • IgA is the main immunoglobulin in secretions - so it's not surprising that patients with
IgA deficiency have more mucosal infections (respiratory, GI, urogenital) than the rest of
the population. What doesn't make sense, at least to me, is that these patients also have
an increase in autoimmune and allergic diseases.
! • Some patients are symptomatic, presenting with recurrent infections and diarrhea.
Others are asymptomatic, and either go undiagnosed for their entire lives, or bump into
the disease in another way: through a blood transfusion. Normal blood has IgA (and all
the other immunoglobulins) in it. If you put normal blood into a patient with IgA
deficiency, the IgA is treated like a foreign antigen, and the patient can develop a severe
(even fatal) anaphylactic reaction.
! 5. List some diseases that are associated with certain HLA alleles:
• There are a lot of these associations. If you don't have time to memorize all of them
(who does?), you might just remember the following two facts (that might be enough to
get through a test question on this stuff):
1. Inflammatory diseases (like ankylosing spondylitis) are generally associated with
HLA-B27
2. Autoimmune diseases (like rheumatoid arthritis and Sjogren syndrome)
tend to be associated with alleles at the DR locus (like DR3 and DR4).
!
6. List features about Sjögren syndrome:
• Lymphocytes infiltrate and damage the patient's lacrimal and salivary glands,
leading to dry eyes and dry mouth.
• It often (but not always) occurs alongside other autoimmune diseases, like
rheumatoid arthritis.
• Patients have a 40x increased risk of developing lymphoma, which is usually in the
salivary gland and usually a mucosa-associated lymphoid tissue (MALT)
lymphoma.
• Most patients have autoantibodies against two ribonucleoprotein antigens: SS-A
 (Ro) and SS-B (La) (and if you have a high titer of SS-A, you're more likely to have
earlier onset of the disease and additional problems, like inflamed joints).
• more common in women has an HLA association (HLA-B8, HLA-DR3, and HLA
DRW52), and has some initiating trigger which is not well-defined.
! 7. What is Goodpasture syndrome? List some of the features:
• It is an autoimmune disease in which patients make autoantibodies against
basement membranes (specifically, against the noncollagenous domain of the
alpha chain of collagen IV).
!
• These autoantibodies destroy basement membranes in the kidney (in the glomeruli)
and lung (in the alveoli), leading to rapidly-progressive glomerulonephritis and
necrotizing hemorrhagic interstitial pneumonitis.
!
• occur more frequently in certain HLA subtypes (specifically, certain subtypes of HLA-
DRB1). The exact thing that kicks off the disease has not been identified, but viral
infection, exposure to hydrocarbon solvents, and smoking have all been proposed as
possibilities.
!
• Most patients are in their teens or 20s, and - unlike just about every other autoimmune
disease you'll learn about - males are affected more frequently than females. The disease
usually presents with hemoptysis (coughing up blood), progressing fairly quickly to renal
failure (which is the most common cause of death). Treatment involves plasmapheresis
(which probably works by removing the autoantibodies) and immunosuppressive
therapy.
! 8. Here are some real-life diseases that are caused by hypersensitivity reactions:
• Type I hypersensitivity: allergies.
• Type II hypersensitivity: autoimmune hemolytic anemia, pemphigus vulgaris,
Goodpasture syndrome, myasthenia gravis, Graves disease.
• Type III hypersensitivity: lupus, post-Streptococcal glomerulonephritis, serum
sickness, the Arthus reaction.
• Type IV hypersensitivity: poison ivy exposure, type I diabetes.
! 9. Describe the mechanism behind type II hypersensitivity and give examples:
• In type II ("antibody-mediated") hypersensitivity, the patient makes antibodies that bind
to an antigen on the surface of some cell, leading to one of three things:
1. macrophage ingestion of that cell
2. complement activation and inflammation
3. cellular dysfunction (for example, if an autoantibody binds to the TSH receptor
on a thyroid epithelial cell, that TSH receptor might not work properly)
• examples: autoimmune hemolytic anemia, pemphigus vulgaris, goodpasture syndrome,
myasthenia gravis, graves disease
! 10. What are the two subtypes of type IV hypersensitivity and give and example of
each?
• since there are two main types of T cells: CD4+ ones (helper T cells) and CD8+ ones
(cytotoxic T cells).
!
• The first subtype, "delayed-type hypersensitivity," involves helper T cells, which
attract macrophages and induce inflammation.
• example: poison ivy.
• The other subtype, "T-cell-mediated cytotoxicity," involves cytotoxic T cells
which come in and kill target cells
 • example: rejection in cells of a transplanted organ
! 11. What is the mechanism behind type III hypersensitivity and give examples:
• called "immune complex" hypersensitivity, where antibodies bind to antigens, forming
complexes which circulate (either through the whole body or in just one area of the
body). The complexes get stuck in vessels, where they stimulate inflammation and cause
tissue damage (and something called necrotizing vasculitis).
! • Examples: systemic lupus erythematosus, post-streptococcal glomerulonephritis,
polyarteritis nodosa, serum sickness, and the Arthus reaction.
! 12. What are the broad categories of types of immunity in the immune system? What are the
key components of each?
• innate immunity (unchanging defence mechanisms present before infection)
• epithelium, phagocytic cells (neutrophils and macrophages), dendritic cells (which
present antigen), natural killer cells, and complement.
• adaptive immunity (changeable defence mechanisms that are stimulated by microbes).
• lymphocytes and their products. It, in turn, is divided into two parts: humoral
immunity (mediated by B cells and antibodies) and cellular immunity (mediated by
T cells).
! 13. What are natural killer cells and how do they function?
• Natural killer cells make up a small percentage (10-15%) of the lymphocytes in the
blood, with their own surface markers (CD16 and CD56).
• they kill infected and malignant cells and don't need prior exposure to these cells. They
are part of the innate arm of immunity - so they are an early line of defence against
infections (viral ones, mostly) and tumors.
!!
!