Robbins Chapter 6 Key Concepts Flashcards

1
Q

Receptor families used in innate immune system

A

Toll-like receptors that recognize microbes and damaged cells

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2
Q

What are the mediators of adaptive immunity

A

lymphocytes and are the only cells that produce specific and diverse receptors for antigens

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3
Q

Characteristics of T cells

A

have TCRs that recognize peptide fragments of protein antigens displayed on MHC cells of APCs

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4
Q

Characteristics of B cells

A

express antibodies that recognize antigens

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5
Q

Plasma cells

A

activated B cells that secrete antibodies

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6
Q

NK cells

A

kill cells that are infected by microbes
kill stressed or damaged cells beyond repair
express inhibitory receptors that recognize MHC on healthy cells so they don’t kill them

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7
Q

APCs function

A

capture microbes and transport them to lymphoid organs and display them for recognition by lymphocytes

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8
Q

Most efficient APC

A

dendritic cells which live in epithelia and most tissues

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9
Q

Generative lymphoid organs

A

bone marrow and thymus

production of mature lymphocytes

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10
Q

Peripheral lymphoid organs

A

lymph nodes, spleen, mucosal lymphoid tissues

where immune response occurs

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11
Q

Innate immunity components

A

epithelial barriers
phagocytes
NK cells
plasma proteins of complement system

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12
Q

Difference between innate immunity and adaptive immunity

A

innate is first response and doesn’t have fine antigen specificity or memory
adaptive develops slower but is more potent and specialized

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13
Q

Cell mediated immunity

A

reaction of T lymphocytes to fight cell-associated microbes

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14
Q

Humoral immunity

A

mediated by antibodies and is effective against extracellular microbes

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15
Q

Extracellular microbes

A

in circulation and mucosal lumens

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16
Q

Cell-associated microbes

A

phagocytosed microbes and microbes in cytoplasm of infected cells

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17
Q

CD4+ helper T cell function

A

help B cells make antibodies
activate macrophages to destroy ingested microbes
stimulate recruitment of leukocytes
regulate immune response to protein antigen

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18
Q

What mediates CD4+ T cells

A

cytokines

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19
Q

CD8+ cytotoxic T lymphocyte function

A

kill cells that express antigens in cytoplasm (virus and tumor cells) and can produce cytokines

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20
Q

Function of antibodies

A

neutralize microbes and block their infectivity
promote phagocytosis and destruction of pathogen
confer passive immunity to neonates

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21
Q

Other names for immediate (type I) hypersensitivity

A

allergic reactions or allergies

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22
Q

What induces immediate hypersensitivity?

A

environmental antigens (allergens) that stimulate strong Th2 responses and IgE production in genetically susceptible individuals

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23
Q

IgE functions

A

coats mast cells by binding Fce receptors

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24
Q

What are the principal mediators of immediate hypersensitivity

A

histamine, proteases, prostaglandins, leukotrienes, and cytokines

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25
Function of the mediators of immediate hypersensitivity
immediate vascular and smooth muscle reactions and late-phase reaction (inflammation)
26
Functions of antibodies
opsonize (coat) cells and target them for phagocytosis
27
How do antibodies recruit phagocytes
phagocytes express receptors for Tc tail of IgG and complement proteins
28
Where do antibodies and immune complexes deposit?
tissues or blood vessels
29
Result of antibody and immune complex deposition
acute inflammation by activating complement or engaging Tc receptors on leukocytes causes tissue damage
30
Cytokine-mediated inflammation process
CD4+ T cells activated by protein antigen and differentiate in Th1 and Th17 and activate IFNy to activate macrophages
31
Results of cytokine-mediated inflammation
tissue damage and promote fibrosis
32
IL-17 in cytokine-mediated inflammation
recruit leukocytes and promote inflammation
33
Classical T cell-mediated inflammatory reaction
delay type hypersensitivity
34
T-cell mediated cytotoxicity process
CD8+ cytotoxic T lymphocytes (CTLs) specific for antigen recognize and kill cell also secrete IFNy
35
Immunologic Tolerance
unresponsiveness to self antigen | *fundamental property of the immune system
36
What happens in Central Tolerance
immature lymphocytes that recognize self antigens in the generative lymphoid organs are killed by apoptosis
37
What happens in Peripheral Tolerance
mature lymphocytes that recognize self antigens in peripheral tissues become functionally inactive, or are suppressed by regulatory T lymphocytes, or die by apoptosis
38
What 2 factors lead to failure of self-tolerance and the development of autoimmunity
1. Inheritance of susceptibility genes | 2. Infections and tissue injury that ay expose self antigens and activate APCs and lymphocytes in the tissue
39
Characteristics of autoimmune diseases
Chronic and progressive and tissue injury occurs
40
What causes SLE
autoantibodies produced against self antigens and formation of immune complexes
41
Role of autoantibodies in SLE
directed against nuclear antigens
42
Disease manifestations of SLE (5)
nephritis, skin lesions, arthritis, hematologic abnormalities, neurologic abnormalities
43
What causes arthritis in SLE
deposition of immune complexes
44
What causes the breakdown of self-tolerance in SLE (3)
nuclear antigens, genetic factors, environmental factors
45
What is Sjogren syndrome
inflammatory disease that affects salivary and lacrimal glands causing dryness of mouth and eyes
46
What causes Sjogren syndrome
autoimmune T-cell reaction against self antigens in the lacrimal and salivary glands viral infection against infects the tissues
47
What characterizes Systemic sclerosis (scleroderma)?
progressive fibrosis involving skin, GI, and other tissues
48
How does fibrosis occur in systemic sclerosis
activation of fibroblasts by cytokines produced by T cells
49
How does the rejection response against solid organ transplants occur?
initiated by host T cells that recognize foreign HLA antigens of the graft
50
4 mechanisms of rejection of solid organ grafts
hyperacute, acute cellular rejection, acute humoral rejection, and chronic rejection
51
Hyperacute rejection of solid organ
preformed antidonor antibodies bind to graft immediately after transplant
52
Acute cellular rejection of solid organ
T cells destroy graft parenchyma by cytotoxicity and inflammatory reactions
53
Acute humoral rejection of solid organ
antibodies damage graft vasculature
54
Chronic rejection of solid organ
dominated by arteriosclerosis caused by T cell activation and antibodies vascular lesions and T cell reactions cause parenchymal fibrosis
55
Treatment of graft rejection
immunosuppressive drugs that inhibit immune responses against the graft
56
Diseases associated with HSC transplantation
graft vs host diseases, and immune deficiency
57
Primary inherited immune deficiency diseases
inherited mutations in genes involved in lymphocyte maturation or function or in innate immunity
58
Results of deficiencies in innate immunity
defects of phagocyte function, complement, and innate immune receptors
59
X-SCID cause
adaptive immunity problem | mutation in common y chain of cytokine receptor
60
X-SCID results
failure of T and B cell maturation failure of IL-7 signaling defective lymphopoiesis
61
Autosomal recessive SCID cause
secondary defect in antibody responses | mutation in gene encoding ADA
62
Autosomal recessive SCID results
failure of T cell development | accumulation of toxic metabolites during lymphocyte maturation and proliferation
63
X-linked Agammaglobulinemia cause
mutation in the BTK gene which encodes B cell tyrosine kinase that is required for maturation signals from pre-B cell and B cell receptor
64
X-linked Agammaglobulinemia results
failure of B-cell maturation
65
Common Variable Immunodeficiency result
defect in antibody production
66
X-linked hyper-IgM syndrome cause
mutation in gene encoding CD40L
67
X-linked hyper-IgM syndrome results
failure to produce isotype-switched high affinity antibodies IgG IgA and IgE
68
X-linked lymphoproliferative disease (XLP) cause
defect in a signaling molecule
69
X-linked lymphoproliferative disease (XLP) result
defective responses against Epstein-Barr virus and lymphoproliferation