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Immunology > Immune response > Flashcards

Immune response Flashcards

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

A

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

24
Q

IL-3

A

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

25
Q

IFN-g

A

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
Q

IL-4

A

Th2 secreted; induces differentiation into Th2 cells, promotes growth of B cells, enhances class switching to IgE and IgG

27
Q

IL-5

A

Th2 secreted; promotes differentiation of B cells, enhances class switching to IgA, stimulates growth and differentiation of eosinophils

28
Q

IL-10

A

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
Q

IFN-alpha and IFN-beta

A

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
Q

T cell surface markers

A

TCR, CD3, CD28

31
Q

T helper cell surface markers

A

CD4, CD40L

32
Q

Cytotoxic T cell surface markers

A

CD8

33
Q

Regulatory T cell surface markers

A

CD4, CD25, Foxp3

34
Q

B cell surface markers

A

Ig, CD19, CD20, CD21, CD40, MHC II, B7 (Drink Beer at the Bar when you’re 21 -> B cells, EBV, CD21)

35
Q

Macrophage cell surface markers

A

CD14, CD40, MHC II, B7, Fc and C3b receptors (enhanced phagocytosis)

36
Q

NK cell surface markers

A

CD16 (bidns Fc of IgG), CD56 (unique NK marker)

37
Q

Hematopoietic cell surface markers

A

CD34

38
Q

Passive immunity

A

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
Q

Active immunity

A

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
Q

Live attenuated vaccine

A

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
Q

Inactivated or killed vaccine

A

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
Q

Hypersensitivity mnemonic

A

ACID (Anaphylactic and Atopic (Type I), Cytotoxic (Antibody-mediated, Type II), Immune complex (Type III), Delayed (Cell-mediated, Type IV)

43
Q

Type I Hypersensitivity

A

within 20 minutes; allergen links IgE on presensitized mast cells and basophils causeing release of vasoactive amines (histamine)

44
Q

Type II Hypersensitivity

A

“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
Q

Type III Hypersensitivity

A

“Type III has an immune complex with 3 things: antigen-antibody-complement”; the 3 things activate complement -> attracts neutrophils -> release lysosomal enyzmes

46
Q

Type IV Hypersensitivity

A

“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
Q

Serum sickness

A

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
Q

Arthus reaction

A

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
Q

Respiratory burst

A

O2-dependent killing, most effective mechanism, HOCL generated in phagolysosomes destroys phagocytosed microbes

50
Q

NADPH oxidase

A

converts O2 to O2- (superoxide)

51
Q

Superoxide dismutase

A

converts O2- (superoxide) to H2O2

52
Q

Myeloperoxidase (MPO)

A

converts H2O2 to HOCl- (bleach)

53
Q

Catalase

A

converts H2O2 to water and oxygen

54
Q

Type I Hypersensitivity disorders

A

allergic and atopic disorders (rhinitis, hay fever, eczema, hives, asthma); anaphylaxis (bee sting, some food/drug allergies)

55
Q

Type II Hypersensitivity disorders

A

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
Q

Type III Hypersensitivity disorders

A

Arthus reaction (swelling and inflammation after tetanus vaccine), SLE, polyarteritis nodosa, poststreptococcal glomerulonephritis, serum sickness

57
Q

Type IV Hypersensitivity disorders

A

contact dermatitis, graft vs host disease, multiple sclerosis, PPD

Immunology (5 decks)

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