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Diseases of Immunity Pt 1 Flashcards

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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
What cells express MHC Class I?
All nucleated cells and platelets
26
What cells express MHC Class II?
antigen presenting cells
27
What antigens do MHC class I peptides recognize?
Intracellular (viral or tumor)
28
What antigens do MHC class II peptides recognize?
Extracellular (allergens or bacterial)
29
How are antigens processed to create MHC Class I peptides?
Ags broken down by proteasome and transported to ER where they are loaded into MHC and moved to the cell membrane
30
What cells recognize MHC Class I?
CD8 cytotoxic T cells
31
How are antigens processed to create MHC Class II peptides?
antigens are broken down by endolysosomal enzymes and vesicles form with the peptides and MHC II
32
What cells recognize MHC Class II?
CD4 helper T cells
33
Regions and chromosome that code for MHC?
6 regions on chromosome 6; HLA-A, HLA-B, HLA-C, HLA-DP, HLA-DQ, HLA-DR
34
Heterogeneity in HLA haplotypes can be recognized in what ways?
differences in fighting off illness, differences in allergic sensitivities
35
Clinical importance of HLA heterogeneity?
transplanted organs, associated autoimmune diseases
36
General overview of cell-mediated immunity
APCs bring back pathogens while expressing MHC-associated peptide antigens, T cells recognize ag, proliferate, differentiate, migrate, and kill
37
MHC Class I evoke what response?
Killing of intracellular pathogens by CD8
38
MHC Class II evoke what response?
extracellular pathogens by CD4 recruitment of macrophages and other T lymphocyte subsets
39
Actions of B lymphocytes in adaptive immune response
humoral immunity and antibody production--neutralization of microbe, phagocytosis, complement activation
40
Naive B cells can differentiate into what types of cells?
Antibody-secreting plasma cell, IgG-expressing B cell, High-affinity Ig-expressing B cell
41
Abs produced by B cells
IgG, High affinity IgG, IgM
42
Actions of Abs produced by B cells
neutralization of microbe and toxins, opsonization and phagocytosis, antibody-dependent cytotoxicity, complement activation
43
T cell dependent humoral immune response involves what two processes?
isotype switching, increasing affinity
44
Features of IgM
First Ig produced, really big and unable to cross placenta
45
Features of IgG
longest half life, important in fetal protection and responsible for hemolytic disease of newborn
46
Features of IgA
Mucosal defense, present in high levels of colostrum, lack of IgA results in an increased number of sinopulmonary infections
47
Features of IgE
Shortest half life, regulates hypersensitivity reactions, high affinity binding to Fc receptor on mast cells, basophils, eosinophils
48
Natural killer cells in Innate immunity
destroy stressed and abnormal cells, turned off with MHC class I expression
49
What inhibits NK cells
Self MHC molecules, class I MHC
50
What activates NK cells?
damaged cells (virus infected cell)
51
What is responsible for antigen receptor diversity?
B and T cell receptors are products of multiple germline and randomized somatic genetic programming
52
Large population of B and T lymphocytes with exact same genes results in....
abnormal clone, neoplasia, lymphoma
53
Hypersensitivity reaction is defined as....
immune reaction to foreign or self antigens that are excessive and harmful
54
Examples of Type I hypersensitivity reactions
seasonal allergies, asthma, food allergies, urticaria, angioedema, anaphylaxis
55
How does a type I hypersensitivity rxn develop?
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
IL-4 involvement in Type I hypersensitivity development
class switching
57
IL-5 involvement in Type I hypersensitivity development
eosinophil activation
58
IL-13 involvement in Type I hypersensitivity reaction
enhanced IgE production
59
Upon repeated exposure to allergen, what will occur in a type I hypersensitivity reaction?
release of mediators from mast cells, immediate hypersensitivity reaction due to vasoactive amines and lipid mediators, late phase reaction due to cytokines
60
Immediate response in Type I hypersensitivity reaction
vasodilation, vascular leakage, smooth muscle spasm
61
Late phase response in type I hypersensitivity reaction
leukocyte infiltration, epithelial damage, bronchospasm
62
Products responsible for early phase Type I hypersensitivity
Histamine, leukotrienes B4, C4, D4, Prostaglandin D2 and PAF
63
Eosinophilic esophagitis
Food ag-driven disease of childhood, recurrent dysphagia, weight loss (cannot effectively swallow)
64
Role as physicians in responding to TI hypersensitivity response
diagnose allergic rxn, treat with airway support and block histamine, identify the allergen
65
Type II hypersensitivity reaction
reactions where antibodies directly react with antigens present on cell surface or ECM (exogenous or auto -antibodies)
66
Three mechanisms of type II hypersensitivity reactions?
phagocytosis, inflammation, cellular dysfunction
67
Basic mechanism of opsonization and phagocytosis in type II hypersensitivity reactions
opsonized cell interacts with phagocyte, phagocyte engulfs cell; thrombocytopenia and anemia
68
Target ag of autoimmune hemolytic anemia
red cell membrane proteins
69
Target ag of autoimmune throbocytopenic purpura
platelet membrane proteins (GpIIb:IIIa integrin)
70
Basic mechanism of inflammation in type II hypersensitivity reactions
damaged tissues cause activation of complement, results in release of C3a and C5a, causing leukocyte migration
71
Rheumatic heart disease mechanism
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
Basic mechanism of cellular dysfunction in type II hypersensitivity reactions
antibodies are directed against cell surface receptors and cause disruption of endocrine and neural signaling
73
Target ag of goodpasture syndrome
noncollagenous protein in basement membranes of kidney glomeruli and lung alveoli
74
Target ag of acute rheumatic fever
strep cell wall antigen, ab cross reacts with myocardial antigen
75
Target ag of myasthenia gravis
Ach receptor
76
Target ag of graves disease
TSH receptor
77
Target ag of insulin-resistant diabetes
Insulin receptor
78
Basic mechanism of type III hypersensitivity reaction
ag-ab complexes form and deposit in tissues, causing damage
79
Serum sickness
type II hypersensitivity reaction, acute form due to non-human protein ag, chronic form due to self-ag
80
Arthus reaction
local type III hypersensitivity reaction
81
Immunofluorescence pattern of Type II hypersensitivity
smooth, linear
82
Immunofluorescence pattern of Type III hypersensitivity
grainy, granular
83
Basic mechanism of type IV hypersensitivity reaction
CD4 response causes cytokine release and inflammation, CD8 response causes a cytotoxic response against Ag on surface of target cell
84
Immune granulomas
type IV hypersensitivity caused by variety of agents capable of producing a T cell response
85
T cell pathogenicity in type 1 DM
ags of pancreatic islet B cells
86
T cell pathogenicity in MS
protein ags in myelin
87
T cell pathogenicity in IBD
enteric bacteria
88
T cell pathogenicity in RA
collagen or citrullinated self proteins, not entirely known
89
TB skin test
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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