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Immunology Flashcards

1
Q

Delayed-type hypersensitivity (Type IV) reactions

A

Mediated by T-lymphs (NO Abs!); 1-2 days afterwards; Ag presented to Th lymph on MHC-II -> IFN-gamma release -> macrophage recruitment –> “walling off…4 T’s - T lymphs, transplant reject, TB test, touching (contact dermatitis). Sarcoidosis

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2
Q

ACID hypersensitivity

A

Anaphylactic and Atopic, Cytotoxic, Immune complex, Delayed

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3
Q

Type I hypersensitivity

A

First and Fast; Free Ag cross-links IgE on pre-sensitized mast cells and basophils -> vasoactive amines (histamine) + tryptase (often used as marker); preformed Ab = fast; delayed = production of leukotrienes.

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4
Q

Type II hypersensitivity

A

Auto-Ab-mediated - IgM and IgG bind to a FIXED Ag on “enemy” cell; Opsonization, complement-mediated lysis (MAC), Ab-dependent cell-mediated death (NK or macros); Goodpastures. Test via Coombs. Direct Coombs test for Ab’s that have bound to patient’s RBC’s. Indirect for Ab’s that could potentially bind RBCs.

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5
Q

Graft-v-host disease

A

Mediated by T-lymphocytes; CD4+, CD8+. Occurs after bone marrow, liver, non-irradiated blood transfusion. 1 week; Rash, jaundice, diarrhea. Helpful for leukemia pts

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6
Q

What immune cell most heavily involved in TB?

A

Caseating granulomas (Langerhans giant cells) mediated by macrophages to present Ag to CD4+ Th1 -> epitheliod cells -> Langerhans giant cells (nuclei in horseshoe)

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7
Q

Cytotoxic T-cell?

A

CD8+ cell. In Eighth grade, “Cuz i’m toxic.” Granzyme B = serine protease.

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8
Q

What region of lymph node enlarged w/ proliferating T-cells?

A

Paracortex

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9
Q

Neutrophil chemotaxis induced by what?

A

IL-8 from macrophages. (Others are leukotriene B, C5a). Movie it [EIGHT] neutrophils! Clean UP on Aisle 8.

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10
Q

What is the f(x) of lymph node follicle?

A

B lymphocyte localization and proliferation. Primary - dense, dormant. Secondary - pale germinal center. In agammaglobulinemia, germinal centers AND primary folicles do not form. B cells are my best friend! (F for follicle). Monoclonal expansion, somatic hypermutation, selection for the best.

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11
Q

Type III hypersensitivity

A

Deposition of IC’s (Antibody-Ag-complement) -> complement activation (C5a) -> neutrophils that damage. Serum sickness, PSGN, lupus nephritis. Arthus reaction (local subacute following intraderminal injection - edema, necrosis, activation of complement)

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12
Q

MHC I

A

Presents ENDOgenous Ag on surface: self, tumor, or Ag 2/2 to viral infection. (Protein, proteasome, RER - where loaded via B2-microglobulin). HLA-A, HLA-B, HLA-C.

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13
Q

MHC II

A

Presents EXOgenous. (Me first, then Outside). Ag taken by APC’s -> Endosomes where meet MHC II - INVARIANT chain -> replaces invariant chain w/ ACIDification + HLA-DM -> presentation to T-helper cells. HLA-DR, DP, DQ. alpha and beta chain (polypeptides).

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14
Q

TxA2 (thromboxane) f(x)?

A

Vasoconstriction, PLT aggregation. TAXIS go in constricted and aggregate areas.

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15
Q

PGI2 f(x)? (prostacyclin)

A

Vasodilation, inhibition of PLT aggregation

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16
Q

T-cell maturation

A

In the thymus. Subcapsular zone - “double negative”. Cortex becomes “double positive” (alphabetaTCR+, CD3+, CD4+, CD8+). Positive selection w/ Cortical epithelial cells to ensure sufficient recognition of its own MHCI and MHC II. Now differentiated to to become single positive CD4 or CD8. Then negative selection by medullary epithelial and dendritic cells to make sure not overly sensitive to self.

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17
Q

Lymph node medulla?

A

Consists of medullar cords (close packed lymphocytes and plasma cells) and medullary sinuses. Macrophages and reticular cells.

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18
Q

Lymph node paracortex?

A

Houses T-cells. Where T and B cells enter from blood. diGeorge underdeveloped. T cells are ParaTroopers.

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19
Q

Para-aortic lymph nodes drain what?

A

Testes, ovaries, kidneys, uterus

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20
Q

GI lymph node drainage system?

A

Celiac for liver, stomach, spleen, pancreas, upper duodenum. Sup. mesenteric for lower duodenum, jejunum, ileum, colon to splenic flexure. Inf. mesenteric for colon from splenic flexure to rectus. Internal iliac for lower rectum to anal canal (above pectinate), bladder, vaginal, prostate.

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21
Q

Spleen dysfunction pathogenesis

A

Decreased IgM -> decreased complement activation -> decreased C3b opsonization -> inc. susceptibility to encapsulated organisms (SHiNE SKiS).

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22
Q

MHC I and MHC II bind to what receptors?

A

Tee Receiving Option #1 AND 2 = OCHO-CUATRO. 1 binds to TCR and CD8+. II binds to TCR and CD4+.

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23
Q

MHC I subtypes associated with disease?

A

HLA B27 = Seronegatives (Psoriatic arthritis, Ankylosing spondylitis, IBD, Reactive arthritis). HLA A3 - hemochromatosis.

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24
Q

MHC II subtypes?

A

DQ2/DQ8 - No Dairy Queen for Celiacs. DR4 = RA, DMI.

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25
Q

CD4+ f(x)?

A

HELPER cells. Helps B cells make antibodies and produce cytokines to activate other immune cells.

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26
Q

Helper cell differentiation?

A

CD4+. IL-12 = Th1. IL-4 = Th2. TGF-B + IL-6 Th17. TGF-Beta-Treg. 2ne1 is number ONE! I Live 4 2.

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27
Q

Co-stimulatory signal for naive T-cell activation by an APC?

A

B7 on dendritic and CD28 on T-cell.

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28
Q

Co-stimulatory signal for Thcell to B-cell?

A

CD40L to CD40.

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29
Q

Th1 v. Th2 (VERY IMPORTANT)

A

1 activates macrophages and cytotoxic T lymphocytes. Secretes IFN-gamma (activates NK, increases MHC expression and Ag presentation). Inhibited by IL-4 and IL-10 from Th2. Th2 recruits eosinophils and promotes IgE production by B cells. Secretes IL-4, 5, 6, 13. Inhibited by IFN-gamma.

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30
Q

Two major sections of antibody structure?

A

Fab - Ag-binding segment, determines idiotype. Fc = c for constant, carboxy, complement binding, carbohydrates side chains. Determines isotype (e.g. IgM).

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31
Q

What immunoglobulins are expressed by mature B lymphocytes?

A

IgM and IgD. IgM produces immediate response to an Ag. Monomer on cell. Pentamer when secreted (to better trap Ag’s).

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32
Q

IgG function

A

Secondary (Delayed) response. Fixes complement, crosses placenta, opsonizes bacteria, neutralizes toxins and viruses.

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33
Q

IgA function

A

Prevents attachment of bacteria and viruses to mucous membranes, Does NOT fix complement. Monomer in circulation but secreted as DIMER. Crosses epithelial cels.

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34
Q

IgE function

A

Binds mast cells and basophils. CROSS-links when exposed to allergen -> type-1 hypersensitivity. Activates eosinophils via an Ab-depedent cellular toxicity (against parasites) where the Eos releases major basic protein and other enzymes. Lowest concentration in serum.

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35
Q

Thymus-independent vs. thymus-dependent Ag’s

A

Thymus-independent Ag’s lack a peptide component and therefore cannot be presented to T-cells via MHC to induce memory. Boosters req. Thymus-dependent Ag’s lead to memory.

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36
Q

Acute-phase reactants are induced by what and produced by what?

A

Induced by IL1, IL6, TNF-alpha, IFN-gamma. Produced by liver

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37
Q

Acute-phase reactans

A

Serum amyloid A, CRP (opsonin, fixes complement and facilitates phagocytosis), Ferritin (binds and sequesters Fe), Fibrinogen (~ESR), Hepcidin (prevents release of iron bound by ferritin). DECREASED albumin and transferrin.

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38
Q

Three ways to activate complement pathway?

A

Classic = classic GM (IgG and IgM). Alternative via microbe surface molecules. Lectin via mannose or other SUGARs.

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39
Q

Complement functions?

A

C3b BINDS bacteria. C3a, C4a, C5a cause Anaphylaxis. C5a also neutrophil chemotaxis. C5b-9 leads to cytolysis via MAC (Gram-NEG like N.). Deficiencies complement can lead to recurrent Neisseria infections.

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40
Q

Inhibitors of complement system?

A

Decay-accelerating factor (DAF) and C1 esterase inhibitor prevent complement activation on self cells

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41
Q

C5-C9 deficiency?

A

Neisseria bacteremia

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42
Q

DAF deficiency?

A

Complement-mediated lysis of RBCs; paroxysmal nocturnal hemoglobunuria. 3 letter DAF = RBC.

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43
Q

C3 deficiency?

A

Increases risk of severe pyogenic sinus and resp tract infections as well as type III hypersensitivity

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44
Q

C1 esterase inhibitor deficiency

A

Hereditary angioedema. ACEi’s contra’d

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45
Q

Interleukin phrase?

A

Hot T-bone stEAK. IL-1 fever. IL-2 stimulates T-cells. IL-3 stimulates bone marrow. IL-4 stimulates IgE (&IgG) production (+ Th2 differentiation). IL-5 stimulates IgA production (activates dos). IL-6 stimulates aKUTE-phase protein production.

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46
Q

Tregs

A

Suppressing inflammation (IL-10 and TGF-Beta).

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47
Q

Interferons

A

Glycoproteins synthesized by virally-infected cells to prime other cells for attack. When dsRNA enters, RNAase L (degrades ALL mRNA) and Protein kinase involved -> apoptosis

48
Q

Epstein Barr Virus

A

Binds CD-21 of B-cell. Drink Beer at a Bar when you’re 21.

49
Q

For what do we provide passive immunity?

A

To Be Healed Rapidly - Tetanus, Botulinum, HBV, Rabies

50
Q

Four type of blood transfusion reactions?

A

Allergic, anaphylactice, febrile nonhemolytic transfusion, acute hemolytic transfusion

51
Q

Allergic vs. anaphylactic blood transfusion reaction

A

Allergic is Type I hypersensitivity against plasma proteins (tx with antihistamines). Anaphylactic leads to dyspnea, bronchospasm, shock. (e.g. IgA deficient ppl must NOT receive blood w/ IgA)

52
Q

Febrile nonhemolytic transfusion reaction

A

Type II HS rxn. autoantibiodies against donor HLA and leuk’s -> fever, HA, chills, flushing.

53
Q

Acute hemolytic transfusion reaction

A

Type II HS against donor RBC’s. Fever, hypotension, flank pain, jaundice, hemoglobinemia

54
Q

Anti-Jo-1, Anti-SRP, Anti-Mi-2

A

Polymyositis, dermatomyositis

55
Q

Scleroderma autoAb’s?

A

Anti-centromere (CREST), anti-Scl070 (topoI, diffuse)

56
Q

Anti-smooth muscle

A

Autoimmune hepatitis

57
Q

Anti-histone

A

Drug-induced lupus

58
Q

Anti-glutamate decarboxylase

A

T1DM

59
Q

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

A

Sjogren

60
Q

c-ANCA v. p-ANCA

A

Wegener’s vs. Microscopic polyangiitis or Churg-Straus

61
Q

IgA antiedomysial, IgA anti-tissue transglutaminase

A

Celiac disease

62
Q

No T-cell susceptibilities?

A

Candida, PCP, CMV, EBV, JCV, VZV, sepsis

63
Q

No B-cell susceptibilities?

A

SHiNE SKiS, enteroviral, encephalitis, poliovirus, giardia

64
Q

B-cell only disorder names? T-cell only disorder names?

A

B’s: X-linked (Bruton Agammaglobulinemia, Selective IgA deficiency, Common variable immunodeficiency. T’s: Thyimc aplasia (digeorge), IL-12 receptor deficiency, Autosomal dominant hyper-IgE syndrome (Job syndrome), chronic mucocutaneous candidiasis

65
Q

X-linked (Bruton) agammaglobulinemia

A

Defect in BTX (RTK) -> NO B-cell maturation. Recurrent bacterial and enteroviral infections after 6 mo (after maternal IgG). Absent/scanty lymph nodes and tonsil. Normal B-cell count but decreased Ig’s.

66
Q

Selective IgA deficiency

A

Unknown etio, but most common primary immunodeficiency. Majority asymptomatic. Airway, GI infections, Autoimmune, Atopy, anaphylaxis to IgA containing products. Only IgA low.

67
Q

Common variable immunodeficiency

A

Defect in B-cell differentiation. Can be acquired in 20’s-30’s. Inc. risk of autoimmune, bronchiectasis, lymphoma, sinopulmonary. Dx w/ decreased PLASMA cells and immunoglobulins

68
Q

Thymic aplasia

A

22q11 del w/ failure to dvpt 3rd and 4th pharyngeal pouches. Tetany (hypoCa), recurrent viral/fungal infections, conotruncal abnl. Dx w/ dec. T-cells, dec. PTH, dec. Ca2+. FISH to detect 22q11 del.

69
Q

IL-12 receptor deficiency

A

AR. Decreased Th1 response (2ne1 is number ONE). Disseminated mycobacterial and fungal. Lab w/ decreased IFN-gamma.

70
Q

Autosomal dominant hyper-IgE syndrome (Job syndrome)

A

Deficiency of Th17 cells b/c of STAT3 mut -> dec. neutrophil recruitment. FATED = coarse Facies, cold staph Abscesses, retained primary Teeth, increased IgE, Dermatologic; Labs with increased IgE and decreased IFN-gamma.

71
Q

Chronic mucocutaneous candidiasis

A

T-cell dysf(x) of many causes. Noninvasive Candida skin and mucous membrane infections. Labs - absence in vitro T-cell proliferation in response to Candida ay’s. Absent cut. run to Candida antigens.

72
Q

Combined B and T cell disorder names?

A

SCID, Ataxia-telangectasia, Hyper-IgM, Wiskott-Aldrich

73
Q

Ataxia telangiectasia

A

Defects in ATM gene = Dbl stranded DNA breaks. Ataxia, spider Angiomas, IgA deficiency. Dx - INC AFP, decreased IgA, IgG, and IgE. Lymphopenia and cerebellar atrophy.

74
Q

Hyper-IgM syndrome

A

Mostly commonly 2/2 defective CD40L -> class-swiching defect. X-linked recessive. Severe pyogenic infections early (PCCP, crypto, CMV). Lymphoid hyperplasia. Labs - Increased IgM but decreased IgG, IgA, and IgE.

75
Q

Wiskott-Aldrich syndrome

A

WAS (X-linked recessive). T-cells unable to reorganize actin. WATER = Wiskott-Aldrich, Thrombocytopenic purport, Eczema, Recurrent infections. Labs - Increased IgE and IgA but decreased/nl IgG and IgM.

76
Q

Leukocyte adhesion deficiency (type 1)

A

Defect in LFA-1 INTEGRIN leading to impaired migration and chemotaxis of phagocytes. AR. Recurrent bacterial skin and mucosal infections, absent pus, impaired wound, DELAYED separation of umbilical cord. Labs - increased neutrophils but absence in infection sites.

77
Q

Chediak-Higashi syndrome

A

Defect in LYSOSOMAL trafficking regulator (LYST) leading to MT dysf(x) in phagosome-lysosome FUSION. AR. Recurrent pyogenic inf by staph and strep. Partial albinism, periphal neuropathy, progressive neurodegen and infiltrative lymphohistiocytosis. Dx w/ giant granules in neutrophils/PLT and pancytopenia.

78
Q

Chronic Granulomatous Disease

A

Defect in NADPH oxidase -> decreased ROS and absent resp burst by neutrophils. Catalase + susceptibility (PLACESS - Pseudo, Listeria, Asper, Candida, E. coli, Staph, Serratia). Dx = abnl dihydrorhodamine flow cytometry (Decreased fluoresence) or nitroblue tetrazolium dye (No change from yellow to dark blue formazan)

79
Q

Types of grafts

A

Auto=self. Syngeneic = identical twin or clone. Allograft = nonidentical individual of same species. Xenograft = different species.

80
Q

Differences between hyper acute and acute transplant rejection?

A

Hyperacute is within minutes and due to pre-existing antibodies against donor ag (type II) leading to complement activation and widespread thrombosis of graft vessels. tx = removal. Acute is within weeks to months and is both cellular (cytotoxics against donor MHC’s) and humoral (auto-Ab’s develop over time) leading to vasculitis of graft vessels. tx = prevent/reverse with immunosuppressants

81
Q

Chronic transplant rejection

A

Takes months to years. Recipient T-cells react against donor MHCs leading to irreversible T-cell and Ab-mediated damage. Heart atherosclerosis. Lung bronchiolitis OBLITERANS. Liver VANISHING bile ducts. Kidney vascular fibrosis and glomerulopathy. Histo - scant inflammatory cells and interstitial fibrosis.

82
Q

Two calcineurin inhibitors?

A

Cyclosporine and tacrolimus. Block IL-2 transcription.

83
Q

Cyclosporine

A

Binds cyclophilin to inhibit calcineurin. Nephrotoxicity! HTN, HLD, hyperglycemia, tremor, hirsuitism, gingival hyperplasia.

84
Q

Tacrolimus

A

Binds FKBP to inhibit calcineurin (which leads to IL-2). Nephrotoxicity!

85
Q

Sirolimus (= Rapamycin)

A

mTOR inhibitor that binds FKBP. Prevents IL-2 signal transduction. (NOT a calcineurin inhibitor) NO nephro. Anemia, thrombocytopenia, leukopenia, insulin resistant.

86
Q

Basiliximab

A

Monoclonal Ab that blocks IL-2R. Edema, HTN, tremor.

87
Q

Azathrioprine

A

Precursor to 6-MP, which –| PRPP amidotranssferase to block purine synthesis. Also used for RA, Crohns, glomerulonephritis. Toxicity is increased by allopurinol b/c 6-MP is degraded by xanthine oxidase. Leukopenia, anemia, thrombocytopenia.

88
Q

Glucocorticoids

A

Inhibits NF-kappaB, suppressing both B and T-cel function by dec. cytokine transcription.

89
Q

Which interferons are used for what diseases?

A

Beta for MS. Gamma for Chronic Granulomatous disease. Alopha for HBV, HCV, kaposi, hairy cell, condyloma acuminatum, renal cell ca, malignant melanoma

90
Q

What drugs to help bone marrow recover?

A

Filgrastim (G-CSF) and sargramstim (GMCSF)

91
Q

Infliximab and adalimumab used for what?

A

TNF-alpha target for IBD, RA, anklylosing spondylitis, and psoriasis.

92
Q

Natalizmab

A

alpha4-integrin. MS and Crohns. (PML risk)

93
Q

Abciximab

A

Glycoprotein IIb/IIIa (II x III = SIXamab). Anti-plt to prevent complications in patients undergoing PCI

94
Q

Denosumab

A

RANKL. used for osteopersosis to inhibit osteoclast maturation.

95
Q

Omalizumab

A

IgE target for asthma.

96
Q

Palivizumab.

A

RSV F protein for ppx for high risk.

97
Q

Trastuzumab

A

HER2/neu for breast ca/gastric ca.

98
Q

Rituximab

A

CD20 for B-cell non-hodgkin lymphoma, RA w/ MTX, and ITP.

99
Q

Cetuximab

A

EGFR. Stage IV colorectal ca. Head and neck ca.

100
Q

Bevacizumab.

A

VEGF for colorectal ca and renal cell ca.

101
Q

Alemtuzumab

A

CD52 for CLL.

102
Q

NK Cells

A

Derived from lymphoid stem cells. Granzymes and performs. Lead to apoptosis of cells. Don’t require thymus. Don’t express CD 4,8,or3. Activated by IFN-gamma and IL-12. Kill cells with DEC. MHC I expression.

103
Q

RF?

A

IgM Ab spcific for Fc component of self-IgG

104
Q

BAL CD4:CD8 ratio?

A

High in sarcoidosis. Low in hypersensitivity pneumonitis and lymphocytic interstitial pneumonia in AIDS.

105
Q

B-cell markers

A

CD19, CD20, CD21

106
Q

Which vaccine type leads to more IgA production?

A

Live vaccines.

107
Q

TNF-alpha

A

Produced by activated macrophages. In low concentrations, mediates local inflammatory response. In high concentrations, mediates a systemic response.

108
Q

Acute serum sickness manifestations and histopath?

A

Fever, pruritic skin rash, arthralgias 1-2 weeks after exposure. Histo - small vessel vasculitis with fibrinoid necrosis and intense neutrophilic infiltration. Low serum C3 and C4 (HS type III)

109
Q

Etios of acute serum sickness?

A

CHIMERIC monoclonal antibodies (-xi-‘s, infliximab, rituximab) or nonhuman immunoglobulins (venom antitoxins), penicillin, TMP-SMX.

110
Q

How does IFN-gamma work in TB?

A

IL-12 secreted by infected macrophages seen by T-cell/NK cell, which secretes IFN-gamma. IFN-gamma binds to RTK on macrophage -> Januse kinase 1 and 2 activation -> nuclear signaling via STAT1 -> enhanced intracellular killing. THEREFORE, IL-12 receptor deficiency -> disseminated mycobacterial and fungal infections.

111
Q

VJ vs. VDJ

A

VJ is light. VDJ is heavy.

112
Q

Somatic hypermutation

A

In activated B-cells of an ongoing response, random point mutations in VHL -> immunoglobulins with higher affinities -< better response

113
Q

How do endogenous antigens get into the RER to bind with MHC I?

A

TAP peptide transporter

114
Q

MHC I vs. MHC II cellular expression?

A

Nucleated cells EXCEPT RBC’s (explains persistent infection) vs. dendritic cells

115
Q

Main strategy with which MHC molecules present a diverse set of antigens?

A

Degenerate binding sites. Secondarily, polymorphisms also increase breadth

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