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immunology Flashcards

1
Q

type 4 delayed hypersensitivity reaction moa

A

doesn’t involve antibodies or complement; occurs 1-2 days after exposure as antigen is taken up by dendritic cells, displayed on MHCII, and stimulate Th1 to release interferon-gamma and attract MO

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2
Q

reactive arthritis triad, age group, and lab finding

A

urethritis, arthritis, and conjunctivitis; young men; HLA-B27

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3
Q

hep B markers of DNA replication

A

HBeAg, HBV DNA

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4
Q

hep B chronic infection lab findings

A

high HBeAg, low anti-HBeAg

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5
Q

eosinophil 2 functions

A
  1. defense against parasites: IgE detects parasites, binds and attracts eosinophil via IgE FcR, euosinophil releases major basic protein to kill parasite; 2. regulate type 1 hypersensitivity rxn (mediated by mast/basophils): by releasing histaminase, which helps reduce severity of atopic reaction
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6
Q

EBV nydus of infection

A

pharyngeal mucosa and tonsillar crypts, then blood

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7
Q

EBV binds to what receptor on what cell?

A

CD-21 (C3d complement receptor) on mature B-cells

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8
Q

EBV histological giveaway

A

CD8+ cells that clinically expand to destroy the virus-infected cells; appear much larger with lots of cytoplasm, eccentrically placed nucleus, and cell membrane that conforms to nearby cell bodies

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9
Q

monocotyes and macrophages: signals identity and serves as LPS receptor

A

CD14

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10
Q

type 1 hypersensitivity: moa

A

initial exposure: develop a wheal and undergo class-switching to IgE specific to antigen; re-exposure will result in cross-linking on the surface of basophils and mast cells, degranulation, and release of histamine, proteases, leukotrienes, prostaglandins, and heparin

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11
Q

TNF-alpha produced by what cells, does what, and is elevated in what diseases?

A

mast cells and macrophages; activation of inflammatory cells (CD4, PMN, fibroblasts, endothelial cells) and apoptosis of tumor cells; increased in inflammatory conditions like RA, psoriatic arthritis

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12
Q

Anti-TNF-alpha IG

A

infliximab, eternacept

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13
Q

toxic shock syndrome moa

A

superantigen that activates large numbers of helper T-cells (release IL-2) and MO (release IL-1 and TNF); cause capillary leakage, circulatory collapse, hypotension/shock, fever, and skin findings

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14
Q

TB: mycobacteria survival strategy

A

hide in MO, able to escape killing and replicate w/i phagollysozomes

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15
Q

TB: macrophage response

A
  1. present antigen to naive Th cells, 2. secrete IL-12 to induce Th1 differentiation (to produce interferon gamma to help MO), and 3. produce TNF-alpha to recruit additional MO to wall bacteria in
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16
Q

TB: histological hallmark

A

epithelioid MO

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17
Q

hep C genetic variation: 2 moa

A

hypervariable region for envelope glycoprotein; no proofreading 3’-5’ exonuclease activity on virion-encoded RNA polymerase

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18
Q

chronic granulomatous dz: moa, pw, dx

A

inactivation of NADPH oxidase leads to decreased oxidative burst and impaired phagocytic intracellular killing; pw recurrent infection with coag + bacteria, lungs, skin, LN, liver involved, w/ diffuse granulomatous formation; dx by measuring PMN superoxide products (DHR flow cytometry or nitroblue tetrazolium test)

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19
Q

Dihydrorhodamine flow cytrometry test

A

measures conversion of DHR to rhodamine (fluorescent green); decreased NADPH activity, decreased fluorescence

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20
Q

Nitroblue tetrazolium test

A

NADPH oxidaises yellow NBT to dark blue; if yellow, then dz positive

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21
Q

What disease presents similarly to chronic granulomatous disease?

A

myeloperoxidase deficiency (normal DHR/NBT test)

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22
Q

Chediak-higashi syndrome: moa, pw

A

AR defect in phagosome-lysosome fusino in PMN, leading to abnormal giant lysosomal inclusions visible on light microscopy; pw recurrent pyogenic infectino by strap, strep, albinism, neurological defects (nystagmus, neuropathy)

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23
Q

NK cell (10 percent of all lymphocytes): function, moa

A

destroy cells w decreased/absent MHCI (virus, tumor); release perforins that punch holes in membranes and granzymes that induce target cell apoptosis

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24
Q

NK cells surface markers

A

CD16, CD56

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25
Q

NK cells activated by

A

interferon gamma and IL-12

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26
Q

Th1 cell-mediated adaptive immunity: moa

A

targets intracellular pathogens, secrets IL-2, interferon- gamma to activates MO and cytotoxic T cells ; also mediates delayed-type hypersensitivity

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27
Q

Th2 cells humoral adaptive immunity: moa

A

secretes IL-4, IL-13 to promote B-cell IgE production, secretes IL-5 to promote eosinophil activity/IgA synthesis

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28
Q

Hypothesis for asthma

A

Increased Th2/Th1 activity; type 1 hypersensitivity, increased IgE

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29
Q

IL-1 secreted by who and stimulates what

A

Secreted by MO to stimulate helper T cells, fever

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30
Q

Acute hemolytic transfusion reaction moa

A

type 2 reaction (antibody-mediated) in which anti-ABO IgM antibodies binds with corresponding antigens on donor RBC, release C5b-C9 (MAC) and C3a-C5a (vasodilation, shock); pw fever, chills, hypotension, chest/back pain, hemoglobinuria, DIC, renal failure;

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31
Q

thymus and t-cell maturation

A
  1. pro t-cells arrive as “double-negative” without CD4, 8 antigens; 2. rearrangement of beta chain of TCR, production of CD4 and CD8 antigens (“double positive”); 3. @ thymic cortex, positive selection picks out T-cells that can bind with MHC cells on thymic epithelial cells (“positive selection”); 4. @ thymic medulla, deletion of t cells that react strongly to self-MHC antigens; 5. loss of CD4 or CD8 antigen
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32
Q

GVH disease

A

m/c after BMT, liver transplant, transfusion of non-irradiated blood; host is severely immunodeficient and donor T cells w/i transplanted tissue recognize host MHC as foreign and attack; pw liver dmg (jaundice, elevated transaminases, alk phos, bili), GI symptoms, and skin desquamation

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33
Q

sarcoidosis moa

A

accumulation of activated MO, formation of noncaseating granulomas (that produce ACE and active vita D), dysregulated cell-mediated immune response (increased CD4/CD8, Il-2, IFN-gamma)

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34
Q

ataxia-telengiectasia moa, pw

A

ATM mutation responsible for DNA break repair; pw ataxia, telengiectasia, immunodeficiency (both cell and humoral) leads to IgA deficiency and respiratory infections

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35
Q

HIV binds to what receptors

A

CD4 and CCR5

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36
Q

langerhans cell

A

derived from myeloid line, dendritic cell in skin/mucosa, professional APC, constitutive expression of MHCII and B7 molecules; histo: “racquet-shaped” cell with intracytoplasmic granules (birbeck)

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37
Q

MO in liver, bone, CNS, kidney, lung

A

kupffer cells, osteoclasts, microglia, mesangial cells, alveolar MO

38
Q

melanocyte

A

NC cells that migrate to epidermal basal layer

39
Q

IgA protease

A

produced by neisseria to cleave IgA and penetrate mucosa (gonorrhea - genitals, meningitis - nasopharynx)

40
Q

IgA secretory form: function, structure

A

Bind to pili and other membrane proteins that mediates bacterial adherence; IgA dimer bound by peptide J chain and peptide secretory component (produce by epithelial cells); abudant in tears, saliva, mucus, colostrum (1st breast milk fed after birth)

41
Q

Protein A: bacteria, moa?

A

Staph A; binds w/ Fc portion of IgG, prevent exposure of C1 domain and direct complement-fixing IgG away from bacteria

42
Q

polysaccharide capsule: bacteria, moa?

A

s. pneumo, n meningitis, h.flu, crypto; impairment of opsonization/phagocytosis

43
Q

interferon type 1 (alpha, beta) moa

A

secreted by infected eukaryotic cells, binds to nreceptors of neighboring cells where it induces transcription of antiviral proteins RNAse L (endonucleases that degrades viral/cellular mRNA) and protein kinase R (phosphorylate and inactivate EF-2, inhibiting translation); these are only active in presence of dsRNA (viral infection)

44
Q

Interferon type 2 (gamme)

A

produced by t cell, nk cells in response to antigens/mitogens; promote TH1 differentiation, improve intracellular killing of MO, increase MHCII enzymes

45
Q

Both type I and type II interferon do what?

A

induce HC1 expression in all cells, stimulate NK, cytotoxic T-cell activity

46
Q

Hyper IgM syndrome: moa, pw, rx

A

2 possible moa: 1. problems with enzyme needed for class switching (DNA recombinase enzyme), 2. CD40T-lymphocyte ligand needed for class-switching is missing; pw recurrent sinus/airway infection 2/2 IgA deficiency; rx with IG

47
Q

Erythroblastosis fetalis/hemolytic dz of newborn

A

if mom is blood-type O, natural antibodies are IgG and can cross placenta (15 percent of pregnancies, and HDN only occurs in 3 percent); can occur with first pregnancy as mom can be exposed to A/B antigen

48
Q

wickott-aldrich moa, pw, rx

A

XLR combined B/T cell disorder, weakness to polysaccharide capsule (S, N, H) and PCP/herpes; pw eczema, thrombocytosis, immunodeficiency; HLA-matched BM transplantation

49
Q

giardia: 2 forms, transmission

A

cysts (infective): oval, 4 nuclei; trophozoite (pathogenic): pear-shaped, multiple flagella, 2 nuclei (“owl eyes”); contaminated water, FO transmission

50
Q

giardia: pw, dx, immune reaction

A

watery diarrhea, malabsorption; stool microscopy for ova, parasites (small bowel biopsy shows villous atrophy); host defends with CD4+ Th cells, secretory IgA production

51
Q

bruton’s agammglobulinemia: moa, lymphoid tissue finding

A

X-linked; mutation to bruton’s tyrosine kinase prevents development of pre-B cells (CD19, 20) into mature, circulating B cells (19, 20, 21) in bone marrow; low/absent B cells in circulation, decreased lymphoid tissue (GC w/i lymphoid follicles are not present normally where B-cells go to proliferate and undergo somatic hypermutation), pan-hypogammaglobulinemia

52
Q

LN structure

A

paracortical zone: T-cell, dendritic cell; outer cortex: house GC; subcapsular regione: lymphatic vessels

53
Q

chronic renal allograft rejection pw

A

worsening HTN, increased Cr, proteinuria

54
Q

RA factor

A

IgM antibody specific for the Fc component of self IgG (like protein A), binds igG to form immune complexes that deposit in synovium and cartilage

55
Q

RA hypothesis

A

autoreactive humoral response against cartilage

56
Q

Inflammation: passage of leukocytes into tissue

A

margination, rolling, activation, tight adhesion, transmigration

57
Q

Inflammation: rolling binds what receptors?

A

PMN (sialyl lewis X/L-selection) to endothelium (E,P selectin)

58
Q

Inflammation: tight adhesion binds what receptors?

A

CD 18/beta-2 integrin (mac-1, LFA-1) on PMN to intercellular adhesion molecule 1 (ICAM-1) on endothelium

59
Q

Inflammation: transmigration requires adhesion to what molecule?

A

platelet endothelial adhesion molecule (PECAM-1)

60
Q

leukocyte adherence deficiency (LAD) type 1 moa

A

absence of CD 18 results in recurrent skin infection w/o pus, delayed umbilical cord detachment, poor wound healing

61
Q

diptheria organism descrption

A

nonmotile, unencapsulated GP rod with metachromatic granules that stain with aniline dyes like methylene blue

62
Q

anti-RH(D) IG

A

IgG anti-Rh antibodies given to Rh- females at 7 months and immediately post-partum to bind with potential Rh factor in children

63
Q

myasthenia gravis: moa

A

circulating antibodies bind with post-synaptic ACh receptor and cause complement-mediated destruction; pw muscle weakness that worsens throughout day; thymus abnormalities

64
Q

Immune system dysfunction in GBS

A

T-cell and macrophage destruction of PNS

65
Q

Immune system dysfunction in polymyositis

A

Tc-mediated SK muscle damage

66
Q

Immune system dysfunction in SLE, RA, CT d/o

A

deposition of immune complexes

67
Q

type II hypersensitivity d/o:

A

MG, good pasture

68
Q

type III hypersensitivity d/o: examples

A

PSGN, hypersensitivity pneumonitis, churg-strauss

69
Q

hypersensitivity pneumonitis

A

IgG precipitates actinomyces antigen, leads to interstitial alveolitis/bronchiolitis

70
Q

type IV hypersensitivity d/o: examples

A

sarcoidosis, contact dermatitis, PPD, candida test

71
Q

complement cascade

A

C1 binding to 2 molecules of IgG or IgM at the Fc region of heavy chain (but only exposed when bound to antigen); easier to begin with IgM

72
Q

silicosis moa, increases susceptibility to what dz?

A

internalized silica particles may disrupt MO phagolysosomes; impair MO killing of intracellular mycobacteria, increased susceptibility to TB

73
Q

Immune system response to TB

A

Mo activates Th1, which releases IFN-gamma to stimulate MO and IL-2 to stimulate cytotoxic T-cell; create caseating granuloma with epithelioid cells, langhans multinucleated cells, fibroblasts, collagen

74
Q

What complement components are needed for formation of MAC? deficiency of these results in increased risk for:

A

C5b - C9; recurrent neisseria infection

75
Q

SCID: 2nd most common cause, rx

A

AR deficiency of adenosine deaminase, which causes toxic levels of adenosine accumulation in lymphocytes; rx retroviral vectors to infect pt stem cells w/ adenosine deaminse gene

76
Q

acute serum sickness: moa, pw, histo, lab

A

type III hypersensitivity; fever, pruritic skin rash, arthralgias 7-14 days after exposure; small vessel vasculitis with fibrinoid necrosis with intense PMN infiltration; decreased C3 level (2/2 IgG/IgM deposition + localized complement consumption)

77
Q

live attenuated flu vaccine moa

A

Stimulate MHCI antigen cells and cytotoxic CD8+ cells

78
Q

FAS sequence: initiator caspases

A

8, 10

79
Q

FAS sequence: executor caspases

A

3, 6 (cleave cellular proteins and activate DNAase)

80
Q

anti-apoptotic signals

A

Bcl-2, Bcl-x

81
Q

Pro-apoptotic signals

A

Bak, bax, Bim (mitocondria becomes permeable and release cytochrome c)

82
Q

This cytokine is produced by macrophages induces PMH chemotaxis and phagocytosis

A

IL-8

83
Q

Granulocytes, present in RS cells

A

CD-15

84
Q

IL-2 secreted by, function?

A

Thcell, growth factor for cytotoxic, helper t cells (via autocrine reaction with IL-2R); also activates monocytes, NK, B-cells; has anti-tumor effects 2/2 increased effectiveness of NK and T cells; rx for metastatic melanoma and RCC

85
Q

Neonatal prophylaxis of tetanus

A

Give pregnant mom shot before birth! IgG antitoxin antibodies across placenta

86
Q

Inhibitory cytokines

A

TGF-beta and IL-10

87
Q

Candida two-part immune response

A
  1. T cells for cutaneous/superficial infection; 2. PMN prevents hematogenous spread
88
Q

polymyositis: two-part injury sequence

A
  1. initial injury releases muscle antigens and triggers inflammatory response 2/2 MO and CD4+; 2. increased expression of MHC on muscle cells increases CD8+ that destroy muscle (thus, histologically see CD8+ lymphocytes and MO in endomyseum); increased creatinine kindase, anti-JO-1 antibodies
89
Q

MHCI structure

A

heavy chain (highly polymorphic) + beta2-microglobulin

90
Q

DiGeorge syndrome moa

A

22q deletion, maldevelopment of 3rd, 4th brachial cleft/pharyngeal pouch; T-cell deficiency 2/2 absence of thymus

91
Q

Asthma MOA and rx for treatment-resistant asthma

A

high IgE response; anti-IgE antibodies (omalizumab)

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