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Step 1 > Immuno > Flashcards

Immuno Flashcards

1
Q

What does thymus come from embryologically?

A

Epithelium of 3rd pharyngeal pouch

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2
Q

What cytokines enhance NK activity

A

IL-2, IL-12, IFN-B, and IFN-a

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3
Q

What part of NK cells binds Fc region of bound Ig to activate cell?

A

CD16

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4
Q

What cytokine triggers Th1 cell differentiation?

A

IL-12

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5
Q

What cytokine triggers Th2 cell differentiation?

A

IL-4

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6
Q

What cytokine triggers Th17 cell differentiation?

A

TGF-B and IL-6

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7
Q

What cytokine triggers Treg cell differentiation?

A

TGF-B

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8
Q

Costimulatory signals for naive T cell activation?

A

B7 with CD28 (CD28 on T cell)

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9
Q

Costimulatory signals for naive B cell activation?

A

CD40L with CD40 (CD40 on B cell, CD40L on T cell)

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10
Q

What cytokines do Th1 cells secrete?

A

IFN-gamma –> activate macrophages and CTLs

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11
Q

What cytokines do Th2 cells secrete?

A

IL-4, Il-5, IL-6, IL-13 –> recurit eosinophils and promote IgE in B cells

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12
Q

What cytokines inhibit Th1 cells?

A

IL-4 and Il-10

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13
Q

What cytokines inhibit Th2 cells?

A

IFN-gamma

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14
Q

What are the cell surface markers for T-Reg cells?

A

CD3, CD4, CD25 (a-chain of IL-2R), and FOXP3 transcription factor

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15
Q

What is C-reactive protein?

A

An acute phase reactant that acts as an opsonin to fix complement and facilitate phagocytosis.

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16
Q

What is hepcidin?

A

An acute phase reactant that prevents release of iron bound by ferritin

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17
Q

Waht triggers the classic pathway for complement?

A

IgG or IgM

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18
Q

What triggers the alternative complement pathway?

A

Microbe surface molecules

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19
Q

What triggers the Lecithin complement pathway?

A

Mannose or other sugars on microbe surface`

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20
Q

What are the two primary opsonins in bacterial defense?

A

C3b and IgG

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21
Q

What keeps complement from activating on RBCs?

A

DAF (CD55) and C1 esterase inhibitor

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22
Q

Complement disorders: C1 esterase inhibitor

A

Causes hereditary angioedema. ACE inhibitors contraindicated

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23
Q

Complement disorders: C3 deficiency:

A

Increased risk pyogenic and respiratory tract infections. Increased susceptibility to type III hypersensitivity reactions.

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24
Q

Complement disorders: C5-C9

A

Susceptibility to Neisseria

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25
Q

Complement disorders: DAF deficiency (GPI anchored enzyme)

A

Paroxysmal nocturnal hemoglobinuria –> complement lysis of RBCs

26
Q

Cytokines: IL-1

A

Macrophages - fever, acute inflammation, activates endothelium, recruit leukocyes, activates osteoclasts

27
Q

Cytokines: IL-6

A

Macrophages and Th2 - fever and production of acute-phase proteins

28
Q

Cytokines: IL-8

A

Macrophages - major chemotactic factor for neutrophils

29
Q

Cytokines: IL-12

A

Macrophages and B cells - induce differentiation to Th1 cells, activate NK cells.

30
Q

Cytokines: TNF-alpha

A

Macrophages - mediate septic shock, activates endothelium, leukocyte recruitment, vascular leak

31
Q

Cytokines: IL-2

A

T cells - stimulates T cell growth

32
Q

Cytokines: IL-3

A

T cells - Growth and differentiation of bone marrow stem cells. Funcitons like GM-CSF

33
Q

Cytokines: IFN-gamma

A

Th1 cells - Antiviral and antitumor properties, activates NK cells, increase MHC expression and antigen presentation in all cells

34
Q

Cytokines: IL-4

A

Th2 cells - induce differentiation into Th2 cells, promotes B cell growth, class switching to IgE and IgG.

35
Q

Cytokines: IL-5

A

Th2 cells - Differentiation of B cells, class switching to IgA, growth and differentiation of eosinophils

36
Q

Cytokines: IL-10

A

Th2 cells - Modualtes inflammatory response, inhibits activated T cells and Th1. Also secreted by Treg cells. (similarities to TGF-B)

37
Q

What is RNAase L

A

Degrades viral/host mRNA in a virlaly infected cell that was “primed” by interferon

38
Q

What are T cell surface proteins?

A

TCR, CD3, CD28 (binds B7)

39
Q

What are B cell surface proteins?

A

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

40
Q

What are macrophage surface proteins?

A

CD14, CD40, MHC II, B7, Fc and C3b receptors

41
Q

Waht are NK cell surface proteins?

A

CD16 (bind Fc of Ig), CD56

42
Q

What are examples of live attenuated vaccines?

A

Measles, Mumps, Rubella, Sabin polio, intranasal influenza, varicella, yellow fever

43
Q

What are examples of killed vaccines?

A

Cholera, Hep A, Salk polio, injected influenza, rabies

44
Q

What is Type I hypersensitivity?

A

Immediate - antibody-mediated

45
Q

What is Type II hypersensitivity?

A

Cytotoxic (antibody-mediated) –> Coombs test, NK cells or mavrophages

46
Q

What is Type III hypersensitivity?

A

Immune complex (antigen-Ab-complement) –> serum sickness, arthus reaction

47
Q

What is type IV hypersensitivity?

A

Delayed T-cell response

48
Q

What gene is mutated in X-linked agammaglobulinemia?

A

BTK - Bruton’s tyrosine kinase

49
Q

What is the most common primary immunodeficiency?

A

Selective IgA deficiency - show anaphylaxis to IgA-containing products

50
Q

What is the underlying abnormality in CVID?

A

Defect in B cell differentiation - can be acquired in 20s and 30s. decrease in plasma cells and Ig. Increased risk of AI disease, bronchiectasis, lymphoma, and sinopulmonary infections.

51
Q

What happens in IL-12 receptor deficiency?

A

Decreased Th1 response. Disseminated mycobacterial and fungal infections, can present after BCG vaccine. Autosomal recessive

52
Q

What is Job syndrome?

A

Autosomal dominant Hyper-IgE. Deficiency of Th17 cells from STAT3 mutation –> impaired recruitment of neutrophils to sites of infection. High IgE, low IFN-gamma. FATED: coarse Facies, Abscesses, retained primary Teeth, igE, Dermatologic problems.

53
Q

What is the underlying problem in chronic mucocutaneous candidiasis?

A

T-cell dysfunction - get noninvasive candidal infection of skin and mucosa.

54
Q

What is Ataxia-telangiectasia?

A

Defects in ATM gene –> DNA ds breaks –> cell cycle arrest. Triad: cerebellar defects, spider angiomas, IgA deficiency. Increased AFP, decreased IgA, IgG, and IgE.

55
Q

What is Hyper-IgM?

A

Defective CD40L - class switching defect, X-linked recessive. Severe pyogenic infections, opportunistic infections.

56
Q

What is Wiscott-Aldrich syndrome?

A

Mutation in WAS gene - T cells unable to reorganize actin cytoskeleton. X-linked recessive. WATER: Wiskott-Aldrich, Thrombocytopenic purpura, Eczmea, Recurrent Infection. Increased AI Dz risk. High IgE and IgA. Fewer and smaller platelets.

57
Q

What is leukocyte adhesion deficiency (type 1)?

A

Defect in LFA-1 integrin (CD18 protein on phagocytes) –> impaired migration and chemotaxis. autosomal recessive. Delayed wound healing, no pus formation, increased neutrophil count in blood, but not at wound site.

58
Q

What is Chediak-Higashi syndrome?

A

Defect in lysosomal trafficking regulator gene (LYST)–> mictrotubule dysfunction in phagosome-lysosome fusion. autosomal recessive. Recurrent pyogenic infectinos, albinism, neurodegeneration. Giant granules in neutrophils and platelets. Pancytopenia. Mild coag defects.

59
Q

What is chronic granulomatous disease?

A

Defect in NADPH oxidase –> no respiratory bursts in neutrophils. X-linked recessive. Susceptibility to catalase + bugs (PLACESSS). Abnormal dihydrorhodamine test. Nitroblue tetrazolium dye test is negative.

60
Q

What is the CD name for Fas?

A

CD95

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