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Immune response Flashcards

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1
Q

Acute phase proteins (upregulated)

A

C-reactive protein (binds C protein of Pneumoccoci), ferritin, fibrinogen, hepcidin, serum amyloid A

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2
Q

Acute phase proteins (downregulated)

A

albumin, transferrin

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3
Q

Classical complement pathway

A

IgG, IgM mediated

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4
Q

Alternative complement pathway

A

microbe surface molecules

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5
Q

MBL complement pathways

A

mannose or other sugars

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6
Q

C3b

A

opsonization, deposits on pathogenic surface and on IgG -> CR1 receptors on RBCs, neutrophil, macrophages, etc

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7
Q

C3a, C4a, C5a

A

anaphylaxis (degranulate mast, basophils, and/or eosinophils); C3a and C5a also are chemotatic for leukocytes

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8
Q

C5a

A

anaphylatoxin and neutrophil chemoattractant

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9
Q

Membrane attack complex

A

C5b-9

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10
Q

Opsonins

A

enhance phagocytosis (neutrophils, macrophages, DCs); C3b and IgG are best

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11
Q

Decay accelerating factor (DAF or CD55)

A

accelerates dissociation of C4b2a and C3bBb (classical/lectin and alternative C3 convertases) on membrane of host cell

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12
Q

Membrane inhibitor of reactive lysis (MIRL or CD59)

A

binds to C5b678 on autologous cells to block binding of C9

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13
Q

C1 esterase inhibitor

A

causes C1r2s2 to dissociate from C1q -> protects complement activation of self cells

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14
Q

C1 esterase inhibitor deficiency

A

causes Hereditary angioedema

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15
Q

C3 deficiency

A

increases risk of severe, pyogenic sinus and respiratory tract infections; increased susceptibility to type III hypersensitivity

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16
Q

C5-C9 deficiencies

A

increases susceptibility to Neisseria bacteria

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17
Q

DAF deficiency

A

causes complement mediated lysis of RBCs and paroxysmal nocturnal hemoglobinuria

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18
Q

IL-1

A

macrophage secreted; causes fever, acute inflammation, activates endothelium to express adhesion molcules, induces chemokine secretion to recruit WBCs

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19
Q

IL-6

A

macrophage secreted; causes fever and stimulates production of acute phase proteins

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20
Q

IL-8

A

macrophage secreted; major chemotatic factor for neutrophils (“Clean up on aisle 8”)

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21
Q

IL-12

A

macrophage secreted; induces differentiation of T cells into Th1 cells, activates NK cells

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22
Q

TNF-alpha

A

macrophage secreted; mediates septic shock, activates endothelium, causes WBC recruitment, vasuclar leak

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23
Q

IL-2

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A

all T cell secrete; stimulates growth of helper, cytotoxic, and regulatory T cells, and NK cells

24
Q

IL-3

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A

all T cell secrete; supports growth and differentiation of bone marrow stem cells. Functions like GM-CSF.

25
IFN-g
Th1 secreted; secreted by NK cells in response to IL-12 from macrophages; stimulates macrophages to kill phagocytosed pathogens; activates NK cells to kill virus-infected cells. Increases MHC expression and antigen presentation by all cells
26
IL-4
Th2 secreted; induces differentiation into Th2 cells, promotes growth of B cells, enhances class switching to IgE and IgG
27
IL-5
Th2 secreted; promotes differentiation of B cells, enhances class switching to IgA, stimulates growth and differentiation of eosinophils
28
IL-10
Th2 secreted; decreases expression of MHC class II and Th1 cytokines, inhibits activated macrophages and dendritic cells, also secreted by regulatory T cells. TGF-B and IL-10 both attenuate the immune response
29
IFN-alpha and IFN-beta
glycoproteins synthesized by virus-infected cells that act locally on uniifected cells, priming them for viral defense by helping to selectively degrade viral nucleic acid and protein
30
T cell surface markers
TCR, CD3, CD28
31
T helper cell surface markers
CD4, CD40L
32
Cytotoxic T cell surface markers
CD8
33
Regulatory T cell surface markers
CD4, CD25, Foxp3
34
B cell surface markers
Ig, CD19, CD20, CD21, CD40, MHC II, B7 (Drink Beer at the Bar when you're 21 -> B cells, EBV, CD21)
35
Macrophage cell surface markers
CD14, CD40, MHC II, B7, Fc and C3b receptors (enhanced phagocytosis)
36
NK cell surface markers
CD16 (bidns Fc of IgG), CD56 (unique NK marker)
37
Hematopoietic cell surface markers
CD34
38
Passive immunity
Given preformed antibodies, onset is rapid but half-life is 3 weeks; IgA in breast milk, IgG crossing placenta, mAb; given after exposure to Tetanus toxin, Botulinum toxin, HBV, Varicella, or Rabies virus ("To Be Healed Very Rapidly")
39
Active immunity
Exposure to foregin antigen, onset is slow but has memory; natural infection, vaccines; combined passive and active immunizations can be given for hepatitis B and rabies exposure
40
Live attenuated vaccine
microorganism loses pathogenicity but can grow -> induces cellular and humoral immunity but may revert back to virulent form; MMR, polio (sabin), influenza (intranasal), varicella, yellow fever
41
Inactivated or killed vaccine
pathogen is inactivated by heat or chemicals -> induces mainly a humoral response and safer but usually need boosters; rabies, influenza (injection), polio (salk), hepatitis A ("RIP Always")
42
Hypersensitivity mnemonic
ACID (Anaphylactic and Atopic (Type I), Cytotoxic (Antibody-mediated, Type II), Immune complex (Type III), Delayed (Cell-mediated, Type IV)
43
Type I Hypersensitivity
within 20 minutes; allergen links IgE on presensitized mast cells and basophils causeing release of vasoactive amines (histamine)
44
Type II Hypersensitivity
"Type II is cy-2-toxic"; IgM, IgG bind to fixed antigen on "enemy" cell -> cell destruction by opsonization/phagocytosis, complement and Fc receptor mediated inflammation, and antibody mediated cellular dysfunction; use direct or indirect Coombs test
45
Type III Hypersensitivity
"Type III has an immune complex with 3 things: antigen-antibody-complement"; the 3 things activate complement -> attracts neutrophils -> release lysosomal enyzmes
46
Type IV Hypersensitivity
"4th and last - delayed, cell-mediated, 1-2 weeks"; T cells encounter antigen and then release cytokines leading to macrophage activation (no antibody); 4 T's: T cells, Transplant rejection, TB skin tests, Touching
47
Serum sickness
Type III hypersensitivity, occurs after 5 days where antibodies to foreign proteins are produced and form immune complexes that deposit in membrane -> fix complement and damage tissue
48
Arthus reaction
Type III hypersensitivity, intradermal injection of antigen induces antibodies, which form antigen-antibody complexes in the skin, characterized by edema, necrosis, and activation of complement; mainly caused by drugs
49
Respiratory burst
O2-dependent killing, most effective mechanism, HOCL generated in phagolysosomes destroys phagocytosed microbes
50
NADPH oxidase
converts O2 to O2- (superoxide)
51
Superoxide dismutase
converts O2- (superoxide) to H2O2
52
Myeloperoxidase (MPO)
converts H2O2 to HOCl- (bleach)
53
Catalase
converts H2O2 to water and oxygen
54
Type I Hypersensitivity disorders
allergic and atopic disorders (rhinitis, hay fever, eczema, hives, asthma); anaphylaxis (bee sting, some food/drug allergies)
55
Type II Hypersensitivity disorders
acute hemolytic transfusion reactions, autoimmune hemolytic anemia, Bullous pemphigoid, erthroblastosis fetalis, Goodpasture syndrome, Graves disease, Guillan-Barre syndrome, Idiopathic thrombocytopenic purpura, myasthenia gravis, pemphigus vulgaris, pernicious anemia, rheumatic fever
56
Type III Hypersensitivity disorders
Arthus reaction (swelling and inflammation after tetanus vaccine), SLE, polyarteritis nodosa, poststreptococcal glomerulonephritis, serum sickness
57
Type IV Hypersensitivity disorders
contact dermatitis, graft vs host disease, multiple sclerosis, PPD

Immunology (5 decks)

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