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MOD > Diseases of Immunity Pt 1 > Flashcards

Diseases of Immunity Pt 1 Flashcards

1
Q

Innate Immunity definition

A

pre-esixting defense against pathogens

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2
Q

Components of innate immunity

A

barrier defense, neutrophils, dendritic cells, NK cells, complement proteins

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3
Q

Adaptive immunity definition

A

specific, programmed defense in response to ag presence

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4
Q

Components of adaptive immunity

A

lymphocytes!!!

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5
Q

Physical barriers of innate immunity

A

skin, ciliated epithelium in tracheobronchial tree

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6
Q

Chemical barriers of innate immunity

A

saliva, tears, gastric acid

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7
Q

Three main PRRs

A

Toll like receptors, NOD-like receptors, C-type lectin receptors

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8
Q

TLRs culminate on what transcription factors?

A

NF-kB and interferon regulatory factors

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9
Q

NOD-like receptors signal via what protein

A

inflammasome

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10
Q

Action of inflammasome

A

activates caspase-1 that cleaves precursor of IL-1 to biologically active form

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11
Q

C-type lectin receptors detect what?

A

Fungal glycans

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12
Q

Reactions of Innate immunity

A

inflammation, antiviral response, complement

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13
Q

Function of bone marrow in adaptive immunity

A

generation of lymphocyte stem cells and B cell maturation, primary site of hematopoiesis

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14
Q

Function of thymus in adaptive immunity

A

maturation of T lymphocytes

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15
Q

Function of lymph nodes in adaptive immunity

A

lymphocytes can interact with APCs and antigens in circulating lymph

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16
Q

Function of spleen in adaptive immunity

A

lymphocytes can interact with blood-borne antigens

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17
Q

Function of MALT in adaptive immunity

A

allow lymphocytes and plasma cells to be in the vicinity of antigens within mouth and intestinal tract

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18
Q

Cellular components of bone marrow

A

erythroid precursors, megakaryocytes, lymphocytes, neutrophils, adipocytes

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19
Q

T cell migration through the thymus

A

cortex to medulla

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20
Q

The medulla contains what types of cells?

A

Maturing T lymphocytes, dendritic APCs, Hassall corpuscles (squamous cell nests)

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21
Q

APCs interacting with lymphocytes in the lymph node trigger what cell processes?

A

t and b cell clonal expansion, b cell differentiation into plasma cells, migration of T cells and plasma cells into circulation

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22
Q

Role of Helper T cell in adaptive immunity

A

activate macrophages, inflammation, activation of T and B lymphocytes

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23
Q

Role of cytotoxic T cells in adaptive immunity

A

killing of infected cell

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24
Q

Role of regulatory T cell in adaptive immunity

A

suppression of immune response

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25
Q

What cells express MHC Class I?

A

All nucleated cells and platelets

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26
Q

What cells express MHC Class II?

A

antigen presenting cells

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27
Q

What antigens do MHC class I peptides recognize?

A

Intracellular (viral or tumor)

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28
Q

What antigens do MHC class II peptides recognize?

A

Extracellular (allergens or bacterial)

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29
Q

How are antigens processed to create MHC Class I peptides?

A

Ags broken down by proteasome and transported to ER where they are loaded into MHC and moved to the cell membrane

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30
Q

What cells recognize MHC Class I?

A

CD8 cytotoxic T cells

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31
Q

How are antigens processed to create MHC Class II peptides?

A

antigens are broken down by endolysosomal enzymes and vesicles form with the peptides and MHC II

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32
Q

What cells recognize MHC Class II?

A

CD4 helper T cells

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33
Q

Regions and chromosome that code for MHC?

A

6 regions on chromosome 6; HLA-A, HLA-B, HLA-C, HLA-DP, HLA-DQ, HLA-DR

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34
Q

Heterogeneity in HLA haplotypes can be recognized in what ways?

A

differences in fighting off illness, differences in allergic sensitivities

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35
Q

Clinical importance of HLA heterogeneity?

A

transplanted organs, associated autoimmune diseases

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36
Q

General overview of cell-mediated immunity

A

APCs bring back pathogens while expressing MHC-associated peptide antigens, T cells recognize ag, proliferate, differentiate, migrate, and kill

37
Q

MHC Class I evoke what response?

A

Killing of intracellular pathogens by CD8

38
Q

MHC Class II evoke what response?

A

extracellular pathogens by CD4 recruitment of macrophages and other T lymphocyte subsets

39
Q

Actions of B lymphocytes in adaptive immune response

A

humoral immunity and antibody production–neutralization of microbe, phagocytosis, complement activation

40
Q

Naive B cells can differentiate into what types of cells?

A

Antibody-secreting plasma cell, IgG-expressing B cell, High-affinity Ig-expressing B cell

41
Q

Abs produced by B cells

A

IgG, High affinity IgG, IgM

42
Q

Actions of Abs produced by B cells

A

neutralization of microbe and toxins, opsonization and phagocytosis, antibody-dependent cytotoxicity, complement activation

43
Q

T cell dependent humoral immune response involves what two processes?

A

isotype switching, increasing affinity

44
Q

Features of IgM

A

First Ig produced, really big and unable to cross placenta

45
Q

Features of IgG

A

longest half life, important in fetal protection and responsible for hemolytic disease of newborn

46
Q

Features of IgA

A

Mucosal defense, present in high levels of colostrum, lack of IgA results in an increased number of sinopulmonary infections

47
Q

Features of IgE

A

Shortest half life, regulates hypersensitivity reactions, high affinity binding to Fc receptor on mast cells, basophils, eosinophils

48
Q

Natural killer cells in Innate immunity

A

destroy stressed and abnormal cells, turned off with MHC class I expression

49
Q

What inhibits NK cells

A

Self MHC molecules, class I MHC

50
Q

What activates NK cells?

A

damaged cells (virus infected cell)

51
Q

What is responsible for antigen receptor diversity?

A

B and T cell receptors are products of multiple germline and randomized somatic genetic programming

52
Q

Large population of B and T lymphocytes with exact same genes results in….

A

abnormal clone, neoplasia, lymphoma

53
Q

Hypersensitivity reaction is defined as….

A

immune reaction to foreign or self antigens that are excessive and harmful

54
Q

Examples of Type I hypersensitivity reactions

A

seasonal allergies, asthma, food allergies, urticaria, angioedema, anaphylaxis

55
Q

How does a type I hypersensitivity rxn develop?

A

DC presents Ag to Naive T cells which are differentiated into Th2 Cells; B cells switch to IgE; Mast cells are prepared by binding IgE to their specific FcERI

56
Q

IL-4 involvement in Type I hypersensitivity development

A

class switching

57
Q

IL-5 involvement in Type I hypersensitivity development

A

eosinophil activation

58
Q

IL-13 involvement in Type I hypersensitivity reaction

A

enhanced IgE production

59
Q

Upon repeated exposure to allergen, what will occur in a type I hypersensitivity reaction?

A

release of mediators from mast cells, immediate hypersensitivity reaction due to vasoactive amines and lipid mediators, late phase reaction due to cytokines

60
Q

Immediate response in Type I hypersensitivity reaction

A

vasodilation, vascular leakage, smooth muscle spasm

61
Q

Late phase response in type I hypersensitivity reaction

A

leukocyte infiltration, epithelial damage, bronchospasm

62
Q

Products responsible for early phase Type I hypersensitivity

A

Histamine, leukotrienes B4, C4, D4, Prostaglandin D2 and PAF

63
Q

Eosinophilic esophagitis

A

Food ag-driven disease of childhood, recurrent dysphagia, weight loss (cannot effectively swallow)

64
Q

Role as physicians in responding to TI hypersensitivity response

A

diagnose allergic rxn, treat with airway support and block histamine, identify the allergen

65
Q

Type II hypersensitivity reaction

A

reactions where antibodies directly react with antigens present on cell surface or ECM (exogenous or auto -antibodies)

66
Q

Three mechanisms of type II hypersensitivity reactions?

A

phagocytosis, inflammation, cellular dysfunction

67
Q

Basic mechanism of opsonization and phagocytosis in type II hypersensitivity reactions

A

opsonized cell interacts with phagocyte, phagocyte engulfs cell; thrombocytopenia and anemia

68
Q

Target ag of autoimmune hemolytic anemia

A

red cell membrane proteins

69
Q

Target ag of autoimmune throbocytopenic purpura

A

platelet membrane proteins (GpIIb:IIIa integrin)

70
Q

Basic mechanism of inflammation in type II hypersensitivity reactions

A

damaged tissues cause activation of complement, results in release of C3a and C5a, causing leukocyte migration

71
Q

Rheumatic heart disease mechanism

A

acute and chronic forms occur due to cross reactive antibodies, molecular mimicry between streptococcal antigen and myocardial ag causes antibodies to attack heart leading to vegetations, pericarditis, etc.

72
Q

Basic mechanism of cellular dysfunction in type II hypersensitivity reactions

A

antibodies are directed against cell surface receptors and cause disruption of endocrine and neural signaling

73
Q

Target ag of goodpasture syndrome

A

noncollagenous protein in basement membranes of kidney glomeruli and lung alveoli

74
Q

Target ag of acute rheumatic fever

A

strep cell wall antigen, ab cross reacts with myocardial antigen

75
Q

Target ag of myasthenia gravis

A

Ach receptor

76
Q

Target ag of graves disease

A

TSH receptor

77
Q

Target ag of insulin-resistant diabetes

A

Insulin receptor

78
Q

Basic mechanism of type III hypersensitivity reaction

A

ag-ab complexes form and deposit in tissues, causing damage

79
Q

Serum sickness

A

type II hypersensitivity reaction, acute form due to non-human protein ag, chronic form due to self-ag

80
Q

Arthus reaction

A

local type III hypersensitivity reaction

81
Q

Immunofluorescence pattern of Type II hypersensitivity

A

smooth, linear

82
Q

Immunofluorescence pattern of Type III hypersensitivity

A

grainy, granular

83
Q

Basic mechanism of type IV hypersensitivity reaction

A

CD4 response causes cytokine release and inflammation, CD8 response causes a cytotoxic response against Ag on surface of target cell

84
Q

Immune granulomas

A

type IV hypersensitivity caused by variety of agents capable of producing a T cell response

85
Q

T cell pathogenicity in type 1 DM

A

ags of pancreatic islet B cells

86
Q

T cell pathogenicity in MS

A

protein ags in myelin

87
Q

T cell pathogenicity in IBD

A

enteric bacteria

88
Q

T cell pathogenicity in RA

A

collagen or citrullinated self proteins, not entirely known

89
Q

TB skin test

A

tuberculin PPD injected intradermally and rxn is assessed 48-72 hours later, sensitized T cells start an inflammatory response resulting in local swelling

MOD (34 decks)

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