Immune responses Flashcards

1
Q

what are acute phase reactants

A

factors whose serum concentrations change significantly in response to inflammation

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2
Q

where are acute phase reactants produced and what cytokines induce their modulation

A

produced in the liver; upregulated by IL-1, IL-6, TNF-alpha and IFN-gamma

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3
Q

name five acute phase reactants that are upregulated in response to inflammation

A

serum amyloid A, CRP, ferritin, fibrinogen, hepcidin

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4
Q

what does C-reactive protein do

A

CRP is an opsonin; it also fixes complement and facilitates phagocytosis

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5
Q

what does ferritin do

A

binds and sequesters iron to hide it from microbes

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6
Q

what lab value does fibrinogen correlate with

A

erythrocyte sedimentation rate

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7
Q

what does hepcidin do

A

prevents release of iron bound by ferritin

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8
Q

what acute phase reactants are downregulated during inflammation

A
  • albumin (downregulated to conserve amino acids for other acute phase reactants
  • transferrin (internalized by macrophages to sequester iron)
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9
Q

which immunoglobulins activate the classic pathway?
alternative pathway?
lectin pathway?

A

IgG and IgM activate the classic pathway
microbial surface molecules activate the alternative pathway
microbial mannose or other surface sugars activate the lectin pathway

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10
Q

what role does C3b play

A

opsonization

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11
Q

what three complement molecules mediate anaphylaxis

A

C3a, C4a, and C5a (C5a is also a chemoattractant)

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12
Q

what complement molecules are needed for formation of the MAC

A

C5b-C9

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13
Q

what is the role of C3b

A

opsonization and clearing immune complexes

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14
Q

what do DAF (decy accelerating factor) and C1 esterase inhibitor do

A

DAF and C1 esterase inhibitor help prevent complement activation on self cells

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15
Q

what disease does C1 esterase cause? and what medication is contraindicated for these patients?

A

angioedema;

ACE inhibitors are contraindicated

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16
Q

what conditions are C3 deficient patients predisposed to?

A

severe sinus and respiratory tract infections, as well as type III hypersensitivity rxns (immune complex)

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17
Q

C5-9 deficiencies predispose to what condition

A

Neiserria bacteremia

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18
Q

what conditions does DAF deficiency predispose to

A

complement-mediated hemolysis and paroxysmal nocturnal hemoglobinuria

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19
Q

what does IL-1 do

A

pyrogen
activates osteoclasts
stimulates endothelium to produce adhesion factors
stimulates chemokine secretion to recruit leukocytes

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20
Q

which cytokines are secreted by macrophages

A

IL-1, IL-6, IL-8, IL-12, TNF-alpha

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21
Q

which cytokines are secreted by all T cells

A

IL-2, IL-3

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22
Q

what’s the mnemonic for IL-1 through IL-6 main functions

A

Hot T-Bone stEAK:
1- hot (pyrogen), 2- T cell stimulation, 3-bone marrow stimulation, 4-IgE production, 5-IgA production, 6-stimulates aKute phase protein production

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23
Q

what does IL-8 do

A

chemotaxis for neutrophils

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24
Q

what does IL-12 do

A

stimulates differentiation of T cells to Th1; activates NK cells

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25
Q

what are the four main function of TNF-alpha

A
  1. mediates septic shock
  2. activates endothelium
  3. leukocyte recruitment
  4. vascular leak
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26
Q

what does GM-CSF do and what interleukin shares a similar function

A

Granulocyte Macrophage- Colony Stimulating Factor promotes growth and differentiation of white blood cells
IL-3 shares this same function

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27
Q

how does interferon gamma work

A

has antiviral and antitumor properties
promotes MHC expression and antigen presenting
activates NK cells to kill viral-infected cells

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28
Q

what else does IL-5 do besides promote IgA class switching

A

promotes differentiation of B cells and eosinophils

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29
Q

what does IL-4 do besides promoting class switching to IgG and IgE

A

promotes differentiation to Th2 cells, promotes growth of B cells

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30
Q

what two cytokines play a big role in downregulating the inflammatory response

A

IL-10 and TNF-beta

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31
Q

what are interferons

A

glycoproteins produced by virally infected cells that prime adjacent cells to be prepared to viral defense

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32
Q

what are the two processes that interferons, produced in response to viral dsRNA, activate in order to induce apoptosis

A

RNAase L (degredation of viral and host RNA)

Protein kinase (degredation of viral and host protein)

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33
Q

what are the T cell surface proteins

A

TCR, CD3, CD28

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34
Q

what two cell surface proteins do T helper cells specifically have

A

CD4, CD40 ligand

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35
Q

what are the B cell surface proteins

A

Ig, CD19, CD20, CD21 (EBV receptor), CD40, MHC II, B7

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36
Q

what are the macrophage surface proteins

A

CD14, CD40, MHCII, B7

Fc and C3b receptors (for enhancing phagocytosis)

37
Q

what are the NK cell surface proteins

A

CD16 (binds Fc portion of IgG)

CD56 (a unique NK cell marker)

38
Q

when does anergy occur

A

T cells become unreactive to self-antigens in the absence of costimulation
B cells can also experience anergy, but it’s not as complete as in T cells

39
Q

how do superantigens work

A

superantigens bind the beta region of the TCR and cross-link it to MHC II on APC leading to T cell release of cytokines

40
Q

name some classic examples of antigenic variation

A

influenza (reassorment)
salmonella (2 flagellar variants)
gonorrhea (variable pilus protein)
trypanosomes (programmed rearrangement)

41
Q

for what infections are preformed antibodies often given to protect the patient post-exposure

A

tetanus, botulinum, rabies, HBV

42
Q

what kind of immunity does a live attenuated vaccine induce

A

cellular immunity; strong, often lifelong immunity

43
Q

name some live attenuated vaccines

A

Sabin polio, varicella, intranasal influenza, MMR, yellow fever

44
Q

what kind of immunity does inactivated or killed vaccines produce

A

humoral immunity

45
Q

name some inactivated or killed vaccines

A

cholera, HAV, Salk polio, influenza injection, rabies

46
Q

what cytokine mediates type I hypersensitivity and how

A

IgE; binds free antigen triggering histamine to produce anaphylaxis

47
Q

what cytokines mediate type II hypersensitivity and how

A

IgG and IgM;
via opsonization, complement activation (along with MACs) and complement-mediated lysis, antibody-mediated destruction via NK cells or macrophages

48
Q

for which type of hypersensitivity would you expect a positive Coomb’s test (either direct or indirect)

A

type II (cytotoxic) hypersensitivity

49
Q

what happens in a type III hypersensitivity reaction

A

serum sickness; immune complex form and deposit in membranes where they fix complement leading to tissue damage

50
Q

what is the Arthus reaction

A

a local, subacute type III hypersensitivity reaction usually seen in experimental settings (a classic example is swelling and inflammation following tetanus vaccine)

51
Q

what is type IV hypersensitivity

A

delayed, T-cell mediated immune response (no antibodies involved) in which the correct sensitized T cell binds the antigen and releases lymphokines to activate macrophages

52
Q

is type IV hypersensitivity transferable via serum

A

no; there are no antibodies involved

53
Q

name some type IV hypersensitivity reactions

A

PPD test, contact dermatitis, transplant rejection (graft vs. host disease), Guillain-Barre, Multiple sclerosis

54
Q

name some type III hypersensitivity reactions

A

Lupus, polyarteritis nodosa, post-streptococcal glomerulonephritis, serum sickness, Arthus reaction

55
Q

name some type II hypersensitivity reactions

A

autoimmune hemolytic anemia, Goodpasture’s, pernicious anemia, ITP, erythroblastosis fetalis (hemolytic disease of the newborn), acute transfusion reactions, rheumatic fever, bullous pemphigoid, pemphigus vulgaris

56
Q

what are some common clinical manifestations of type I hypersensitivity reactions

A

allergic rhinitis/ hay ever, eczema, hives, asthma

57
Q

what is the clinical presentation of anaphylactic reaction

A

hypotension/ shock, hives, bronchospasm, dyspnea / respiratory arrest

58
Q

what’s the difference between targets of febrile nonhemolytic and acute hemolytic transfusion reactions

A

febrile nonhemolytic: targets are HLA antigens and leukocytes

acute hemolytic: RBC antigens (ABO incompatibility)

59
Q

name the disorder associated with ACh receptor auto-antibodies

A

myasthenia gravis

60
Q

name the auto-antibody associated with Goodpasture’s syndrome

A

anti-basement membrane antibodies

61
Q

what antibodies are associated with lupus anticoagulant syndrome

A

antiphospholipid antibodies

62
Q

what antibodies are associated with limited scleroderma (CREST syndrome)

A

anti-centromere antibodies

63
Q

what does the acronym CREST denote

A

calcinosis, Raynaud’s phenomenon, esophageal dysmotility, sclerodactyly (tickening and tightening of the skin in localized regions leading to ulcers), telangectasias

64
Q

antidesmoglein antibodies are associated with what condition

A

pemphigus vulgaris

65
Q

what antibodies are associated with SLE

A

antinuclear antibodies, anti-dsDNA antibodies, anti-Smith antibodies, antihistone antibodies (drug-induced SLE), anti-cardiolipin antibodies

66
Q

anti-glutamate decarboxylase antibodies are associated with what condition

A

type 1 diabetes mellitus

67
Q

what antibodies are associated with bullous pemphigoid and what does the molecule targeted normally do

A

anti-hemidesmosome;
hemidesmosome normally anchors the epithelial cell to the basement membrane by connecting the keratin in basal cells to BM

68
Q

what antibodies are associated with polymyositis and dermatomyositis

A

anti-Jo 1, anti-SRP (signal recognition particle), anti-Mi-2

69
Q

what condition is caused by anti-microsomal and antithyroglobulin antibodies

A

Hashimoto’s thyroiditis

70
Q

what antibodies cause primary biliary cirrhosis

A

antimitochondrial antibodies

71
Q

what condition is associated with anti-Scl-70 (anti-DNA topoisomerase I)

A

scleroderma (diffuse)

72
Q

what do anti-smooth muscle antibodies cause

A

autoimmune hepatitis

73
Q

what antibodies are associated with Sjogren’s syndrome

A

anti-SSA (anti-Ro), anti-SSB (anti-La)

74
Q

what antibodies is associated with Grave’s disease

A

anti-TSH receptor

75
Q

what condition is associated with anti-U1 RNP (ribonucleoprotein)

A

mixed connective tissue disease

76
Q

what disease is c-ANCA (PR3-ANCA) positive

A

granulomatosis with polyangitis (Wegner’s)

77
Q

what disease is p-ANCA (MPO-ANCA) positive

A

microscopic polyangitis and Churg-Strauss syndrome

78
Q

what antibodies are associated with Celiac disease

A

IgA antiendomysial, IgA anti-tissue transglutaminase

79
Q

what antibodies are associated with rheumatoid arthritis

A

rheumatoid factor (commonly IgM antibodies that are specific to IgG Fc region) anti-CCP (citrullinated protein)

80
Q

what kind of bacterial infection are you most susceptible to if you have no T cells

A

sepsis

81
Q

what kind of bacterial infection are you most susceptible to if you have no B cells

A

encapsulated bacteria (SHiNE SKiS): strep pneumo, H. flu, Neisseria meningiditis, E. coli, Salmonella, Klebsiella, GBS

82
Q

what bacterial infections are you most susceptible to if you have no granulocytes

A

Staph, Burkholderia cepacia, Serratia, Nocardia

83
Q

what bacterial infection are you susceptible to if you have no complement

A

Neisseria (due to no membrane attack complexes)

84
Q

what viral infections are you most susceptible to if you have no T cells

A

CMV, EBV, JCV, VZV, chronic infections with respiratory and GI viruses

85
Q

what viral infections are you most susceptible to if you have no B cells

A

enteroviral encephalitis, poliovirus (live vaccine contraindicated)

86
Q

what fungi are you most susceptible to if you have no T cell

A

Candida and PCP

87
Q

what parasites are you most susceptible to if you have no B cells

A

GI giardiasis (no IgA)

88
Q

what fungi are you most susceptible to if you have no granulocytes

A

Aspergillus and Candida

89
Q

________ deficiencies cause more recurrent bacterial infections whereas ___________ deficiencies cause more fungal/ parasite infections

A

B-cell deficiences cause more recurrent bacterial infections whereas T cell deficiencies cause more fungal/ parasite infections