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General Pathology Theory > Immunology > Flashcards

Immunology Flashcards

0
Q

Name the components of innate immunity

A
  • Epithelial barriers
  • Phagocytic cells (macrophages, neutrophils)
  • Dendritic cells
  • Natural Killer cells
  • Plasma proteins (complement system, mannose binding lectin, C-reactive protein)
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1
Q

Name 3 HLA alleles and their associated inflammatory diseases

A

B27 : Ankylosing spondylitis, postgonoccoal arthritis, acute anterior uveitis
DR4: Rheumatoid arthritis
DR3: Chronic active hepatitis, Sjogren syndrome, Type 1 DM
HLA-BW47: 21-hydroxylase deficiency

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2
Q

What are the functions of the components of the innate immune system?

A
  • Skin barriers: mechanical barrier of entry by microbes, anti-microbial molecules (defensins)
  • Monocytes/neutrophils: rapidly recruited to site of infection; ingest microbes (recognise molecules released by injured cells, Toll-like receptors, mannose, opsonins) activate NF-kB and increase cytokine production
  • Dendritic cells: produce type 1 interferons, antiviral cytokines inhibiting viral replication and infection
  • NK cells: mediate antiviral defense by stimulating macrophages
  • complement: opsonization, triggers adaptive immune system
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3
Q

Name 3 types of lymphocytes and their function.

A 
B lymphocytes: differentiate into plasma cells, secrete antibodies in response to microbe
CD4+ Helper T: recognize phagocytosed antigen, secrete cytokines to activate macrophages, attract leukocytes, stimulate B lymphocytes to produce antibody (MHC class 2)
CD8+ cytoxic T: Recognize infected cells and kill them (MHC class 1)
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4
Q

What are the components of adaptive immunity?

A

Humoral immunity: protects against extracellular microbes, B-cell lymphocytes sand antibodies
Cell-mediated: defense against intracellular microbes, T-cell lymphocyte mediated, effector T and memory cells

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5
Q

What is the makeup of a T-cell receptor complex?

A
  • Disulfide linked heterodimer, made up of alpha and beta polypeptide chain, each with variable region and constant region
  • linked non-covalently to 5 polypeptide chains, forming the CD3 complex and the xi chain dimer (invariant)
  • other proteins expressed to assist complex include CD4, CD8, CD2, integrins, CD28
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6
Q

What is the role of the T-cell receptor and how does it acquire its function?

A
  • The AB TCR recognizes peptide antigens that are displayed by MHC molecules on the surfaces of APC
  • TCR diversity generated by somatic rearrangement of genes coding for TCR A and B genes, during T-cell development in thymus
  • Enzyme mediating recombination is RAG-1, RAG-2 (recombination activating genes)
  • Individuals able to recognize wide variety of antigens
  • T cells recognize both the antigen-MHC complex and signals provided by APCS
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7
Q

What are the components of the B-cell antigen receptor complex?

A
  • Membrane-bound antibodies (IgM, IgD) are present on surface of all mature, naive B cells bind the antigen
  • Unique antigen specificity determined by RAG-mediated gene rearrangement
  • Two invariant proteins called Igalpha and IGbeta, essential for signal transduction through antigen receptor
  • other molecules include complement receptors, FC receptors, CD40
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8
Q

Name 2 types of dendritic cells, location and their functions.

A
  1. Interdigitating dendritic cells: antigen presenting cells, express microbe-capturing receptors, recruitment to T-cell zone of lymphoid tissue, activation of CD4+ T cells. Located in skin (Langerhans) and intersitium.
  2. Follicular dendritic cells: Fc receptors for IgG and C3b and trap antigen bound to antibodies/complement. Present antigen to B cells. Found in germinal centres of lymph nodes/spleen.
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9
Q

Name 3 functions of macrophages.

A
  • function as APCs after phagocytosing microbes
  • kill ingested microbes after T cell activation (cell mediated)
  • phagocytose and destroy opsonized microbes (IgG/C3b) (humoral)
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10
Q

Outline the function and regulation of NK cells

A
  • Ability to kill infected and tumor cells without prior exposure to these cells AND to lyse IgG coated target cells
  • Express CD16 and CD56
  • regulated by signals from activating and inhibitory receptors
  • Inhibitory: recognizes Self class 1 MHC, not activated
  • Activation: NKG2D receptor recognizes cells damaged by infection/DNA damage, reduced self class 1 MHC=killing
  • Secrete cytokines (interferon gamma) to activate macrophages
  • IL2, IL-15 stimulate proliferation of NK cells
  • IL-12 activates killing and production of interferon gamma
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11
Q

Name chemokines involved in migration of T cells

A
  • L-selection, integrin on high endothelial venules to get Naive-T to lymph nodes
  • CCL-19, CCL21 bind to CCR7 on T cells, enhacing adhesion and inducing migration through endothelial wall
  • E-selection, P-selectin, integrins, CXCL10 to get activated T to site of infection
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12
Q

Describe the 2 classes of MHC molecules and their structure

A
  • Role is to display peptide fragments of proteins for recognition by antigen-specific T-cell
  • genes encoding MHC on chromosome 6
  • MHC 1, MHC2 and genes encoding complement components, TNF, lymphotoxin
  • MHC1: all nucleated cells and platelets, 3 loci: HLA-A, HLA-B, HLA-C
  • Heterodimer of polymorphic alpha (hc) and non-polymorphic beta
  • Extracellular alpha has 3 domains: A1, A2, A3 (binding in cleft formed by A1/A2
  • Display peptides derived from viral antigens found INSIDE cells, and are recognized by CD8+ T lymphocytes. CD8 is a coreceptor.
  • MHC 2: 3 loci HLA-DP, HLA-DQ, HLA-DR.
  • Heterodimer of Alpha and Beta chains, both polymorphic
  • extracellular variable regions have a1, A2, B1, B2 with A1/B1 binding cleft
  • Present antigens internalized into vesicles by endoytosis, usually extracellular microbes and soluble proteins
  • B2 domain has binding site for CD4, respond to T-cell help
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13
Q

Name 5 cytokines of innate immunity and 5 of adaptive immunity

A

Innate: TNF, IL-1, IL-12, Type 1 interferons IFN gamma (made by macrophages, dendritic cells, NK)
adaptive: IL-2, IL-4, IL-5, IL-17, IFN-gamma (made by CD4 T cells)

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14
Q

What are the main steps in cell mediated immunity?

A
  • Antigen capture and transport to lymphoid organs by dendritic cells
  • Antigen recognition in lymphoid organs (CD4+ helper and CD8+ cells cytotoxic)
  • T cell proliferation and differentiation (Naive T cell–>APC–>IL-2–>differentiation in to effector and memory T cells)
  • Differentiated effector and memory T cells enter circulation
  • Migration of effector T- cells to site of antigen
  • CD4+ ( Th1 and TH17 recognize phagocytes with microbes, secrete cytokines leading to recruitment of inflammatory cells, macrophage activation and killing of microbes)
  • CD8+ (CTLs recognize MHC2-cells, kill infected cells)
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15
Q

Name 3 types of helper T cells, cytokines produced, reactions triggered, microbes affected, role in disease

A

TH1: IFN-gamma, activates macrophages, stimulates IgG, good for intracellular microbes, role in autoimmune disease
TH2: IL-4, IL-5, IL-14, stimulates IgE, activates mast cells and eosinophils, good for helminths, role in allergies
TH17: Il-17, IL-22chemokines, recruits neutrophils and monocytes, good for extracellular bacteria and fugi, role in autoimmune disease

16
Q

Describe the main steps in humoral (B-cell mediated) immunity

A
  • Naive B cell is confronted with microbe, expresses IgM and IgD
  • TH express CD40 ligand and cytokines=activate B cells
  • B cells proliferate and differentiate into antibody secreting cells, with class switching depending on the type of microbe (IFN-gamma, IL4)
  • Affinity maturation=improves quality of humoral response
  • Memory cells also generated
  • Antibody secreted: neutrolizes microbes/toxins, opsonizes for phagocytosis (recognition of FC portion of IgG by macrophages and NK cells), activates complement, induces inflammation
17
Q

What are specific roles of isotypes of antibodies?

A
  • IgM: polysaccharides/lipids, neutrolizes microbes/toxins and activates complement
  • IgG: activates complement, Fc portion recognized by NK cells and phagocytes, crosses into placenta and protects fetus
  • IgA: secreted by mucosal epithelia, neutrolized microbes in lumens of GI/respiratory tract
  • IgE: works with eosinophils to kill parasites, by release of eosinophil granule (TH2 cells secret cytokines to stimulate IgE)
18
Q

Classify hypersensitivity reactions, name a representative disorder, give immune mechanism and pathologic lesions

A

Type 1: Immediate hypersensitivity, anaphylaxis, production of IgE antibody=release of vasoactive amines and mast cell mediators followed by recruitment of inflammatory cells. Lesions include vascular dilation, edema, smooth muscle contraction, mucous, tissue injury
Type 2: Antibody mediated, Goodpasture syndrome, production of IgG, IgM=biding of antien on target cell, phagocytosis of target cells or bc of complement or FC receptor, recruitment of neutrophils. Lesions include phagocytosis/cell lysis, inflammation
Type 3: Immune-complex mediated, Lupus, serum sickness, Deposition of antigen-antibody complexes=complement activation, recruitment of leukocytes, release of enzymes. Lesions include necrotizing vascuylitis, inflammation
Type 4: Cell mediated (delayed), contact dermatitis, IBD. Activated T lymphocytes=release of cytokines and macrophages activated, T-cell mediated cytotoxicity. Lesions include perivascular infiltrates, edema, granulomas

19
Q

Describe the sequence of events in type 1 hypersensitivity reactions

A
  1. Exposure to allergen
  2. Activation of TH2 cells and IgE class-switching in B cells
  3. Production of IgE by B cell
  4. Binding of IgE to FC portion of E receptor on mast cells
  5. Repeat exposure to allergen
  6. Activation of mast cell and release of pre-formed mediators
    (mediators include vasoactibev amines, lipid mediators and cytokines)
  7. Immediate hypersensitivity reaction (vasoactive amines) and late-phase reaction (cytokines)
20
Q

Other than IgE, what are other mast cell secretatogues?

A
  • Complement components C5a and C3a
  • Chemokines (IL-8)
  • Drugs (codeine, morphine, adenosine)
  • Physical stimuli (heat, cold, sunlight)
21
Q

Name some mediators produced by activated mast cells

A

A. Granule contents: Histamine, proteases (vasodilation, vascular leakage)
B. Lipid mediators: leukotrienes (*most potent vasoactive, also highly chemotactic), prostaglandin D2 (bronchospasm, mucous) platelet activating factor (platelet activation, bronchospasm)
C. Cytokines (late phase, leukocyte infiltration, epithelial damage, bronchospasm)

22
Q

Describe 3 mechanisms of antibody-mediated injury

A
  1. Opsonization of cells by antibodies and complement components, with ingestion by phagocytes
  2. Inflammation induced by antibody binding to FC receptors of Ig molecules on leukocytes, and complement breakdown products
  3. Anti-receptor antibodies disturb normal function of receptors
23
Q

Name 3 examples of antibody-mediated hypersensitivity (Type 2)

A

A. Transfusion reaction: cells from incompatible donor react and are opsonized by pre-formed host antibody
B. Hemolytic disease of newborn (erythroblastosis fetalis): antigenic difference between mother and fetus, antibodies from mother cross placenta and cause destruction of fetal RBCs
C. Autoimmune hemolytic anemia/agranulocytosis/thrombocytopenia, where antibodies are created to own blood cells
D. Drug reactions where drug attaches to cell surface and Abs are created to the complex

24
Q

Gives 6 examples of antibody mediated diseases (Type 2 rxns)

A
  • Autoimmune hemolytic anemia
  • Autoimmune thrombocytopenic purpura
  • Pemphigus vulgaris
  • ANCA vasculitides
  • Goodpasture syndrome
  • Acute rheumatic feber
  • Myasthenia gravis
  • Graves’ disease
  • IDDM
  • Pernicious anemia
25
Q

Give 5 examples of type 3 (immune complex mediated) hypersensitivity, antigen involved and clinical manifestations

A
  • SLE: nuclear antigens, nephritis, arthritis, skin lesions
  • Post-streptococcal glomerulonephritis: Strep cell wall antigens, nephritis
  • Polyarteritis nodosa: HBV antigens, systemic vasculitis
  • Reactive arthritis: bacterial antigens, acute arthritis
  • Serum sickness: various proteins, arthritis, vasculitis, nephritis
  • Arthus reaction: various proteins, cutaneous vasculitis
26
Q

Describe the mechanism of immune complex mediated hypersensitivity

A
  • Antibody-antigen complexes produce tissue damage by eliciting inflammation at the sites of deposition
  • reaction initiated when antigen combines with antibody in circulation and is deposited in vessel walls
  • antigens can be endogenous or exogenous, and deposition can be systemic or localized (eg. kidney, skin, joints).
27
Q

What factors are involved in formation and deposition of immune complexes?

A

Formation: introduction of protein antigen triggers immune response, antibodies are formed ~7d after exposure, secreted into blood and react with antigen
Deposition: local vascular alterations, medium-sized complexes, antigen excess, organs where blood is filtered at high pressure to make another fluid (kidney,synovium)

28
Q

Describe the components (including cytokines) involved in delayed-type hypersensitivity reactions

A

APC cell presents to CD4+ T-cell
TH1 subset–> produces cytokines IFN-gamma, TNF–>macrophages activation and inflammation
TH17 subset–> produces cytokines IL-17, IL-222–> activate neutrophils
CD8+ cells: detect antigen within cells, leading to cell killing and tissue injury

29
Q

Give 5 examples of T-cell mediated (type 4) hypersensitivity rxns, antigen, and clinical features

A
  • Type 1 DM: pancreatic islet B cells–>chronic inflam in islets, B-cell destruction, diabetes
  • Multiple sclerosis: protein antigens in CNS myelin (myelin basic protein)–> demyelination in CNS with perivascular inflammation
  • Rheumatoid arthritis: antigen in joint synovium ? type 2 collagen–> chronic arthritis with inflammation
  • Crohn disease: unknown, ? bacterial–> chronic intestinal inflammation
  • Contact dermatitis: various environmental antigens–>skin inflammation with blisters
30
Q

List immune mediated inflammatory diseases under ab/immune complex and T-cell mediated

A

AB:hemolytic anemia, thrombocytopenia, myasthenia gravis, Graves’ disease
Immune complex: SLE, polyarteritis nodosa
T cell: DM-1, MS, RA, Sjogren, IBD, inflammatory myopathies

31
Q

What gene is the most frequently implicated in autoimmunity?

A

PTPN-22, encodes protein tyrosine phosphatase and is associated with rheumatoid arthritis, DM-1, others
Polymorphisms in gene encode functionally defective, which cannot regulate tyrosine kinases, leading to excessive lymphocyte activation

32
Q

What is the role of susceptibility genes in autoimmune disorders?

A
  • Multigenetic
  • HLA genes are associated
    ? particular MHC alleles affect negative selection of T ell in thymus OR regulatory T cells (unproven)

General Pathology Theory (6 decks)

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