Immunology Flashcards

1
Q

Immunohematology:

  1. ) A Blood: Possible genotype? RBC Antigen? Ab’s in plasma? Can donate? Receive? Common?
  2. ) B Blood: Possible genotype? RBC Antigen? Ab’s in plasma? Can donate? Receive? Common?
  3. ) AB Blood: Possible genotype? RBC Antigen? Ab’s in plasma? Can donate? Receive? Common?
  4. ) O Blood: Possible genotype? RBC Antigen? Ab’s in plasma? Can donate? Receive? Common?
    - Isohemoglutanins? Primarily made of? When you first come into contact? On each cell type? Ab’s to these? Bombay? Blood match? Typed as?
A
  1. ) AA, AO; A; Anti B; A & AB; A & O; 42%W,27%B
  2. ) BB, BO; B; Anti A; B & AB; B & O; 9%W, 21%B
  3. ) AB; A, B; None; ABonly; A,B,AB, O; 3%W; 4%B
  4. ) OO, Bombay; None; Anti A/ Anti B; A,B,AB,O; O only; 46%W; 48%B
    - Blood antigens primarily glycolipids (lipid backbone with terminal sugar); young in nature; H, A, B, h; IgM made against what you don’t have; LAck transferase gene that places final sugar so does not express even H; Only bombay; “O” but have antigens to O, A, B in plasma
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2
Q

Immunohematology:

  • Cross match: Blood tested for? (7) Reverse typing? 1.) Plasma of patient mixed with? Testing for? 2.) Direct anti-globulin test to check for?
  • Direct antiglobulin test? Detects?
  • Indirect anti-globulin test? Detects?
  • Heterophile ab? Ex? (2)
  • Hemolytic Blood Disease: Consequences? (3)
    1. ) Erthro. Fetalis: Genotypes? Happens why? Type of Ab’s? Prevention? Given when?
    2. ) ABO hemolytic disease: Occurs when? Common in what group?
A
  • ABO, Rh, Hep B, C, HIV, WNV, Syphallis; Add patients serum to RBC’s to test for Ab’s; RBC’s of donor; IgM; IgG
  • Take RBC’s, wash them, add sheep anti-globulin, checks if ab’s on cell in vivo
  • Take RBC’s, add patient plasma, add sheep anti globulin; is there Ab to RBC’s in recipients plasma
  • Ab to one antigen cross reacts to another; Mono ab reacts with sheep blood; syphallis ab reacts with phospholipids of beef heart
    1. ) Rh(+) kids with Rh(-) mom; 3rd trimester has some RBC’s cross placenta and mom makes IgG ab’s which is fine for first kid, but bad there after; Give mom IgG ab to Rh immunoglobulin (Rhogam) before she makes immune response; 28 weeks
  • Mom makes IgG isohemglunins to B blood; (O)
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3
Q

Immunomodulators:

  • Biological response modifiers? Ex? (3)
  • Monoclonal ab’s: Made how?
  • 1st gen? Made from? Works? Gene? Drugs?
  • 2nd gen? Made from? Leads to? Drugs?
  • 3rd gen? Made from? Leads to? Drugs?
  • 4th gen? Made from? Drugs?
  • MAB’s often made against?
A
  • Mimics things body does naturally; receptor antagonist, cytokine, ab
  • Progeny of a single B cell that has been fused with multiple myeloma plasma tumor cell
    1. ) Pure mouse; works first time then Human Against Anti Mouse AB (HAMA); murine; (omab)
    2. ) Chimeric: Only Vh and VL are mouse; leads to HACA; chimeric (ximab)
    3. ) Humanized; only HVR’s are mouse; leads to HAHA; humanized (zumab)
    4. ) SCID mouse with human immune organs; all human; human (umab)
  • TNFa, IL1, anti inflamm agents
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4
Q

Immunomodulators:

  • NK cells: Type of lymphocytes? Work similar to? But? Why? 2 tricks: 1? Part of what response? 2? Ex? Implications with MHC? Have what receptor?
  • Chimeric Antigen receptors: Combine 2 single chain? What are the 2?
  • Cancer therapy with MAB’s: 4 ways this is done?
A
  • Large granular; CTL but no VDJ regions since not from thymus; 1.) Have a few markers to see if cell is stressed (innate response) 2.) Ab dependent cell mediated toxicity (ADCC): Tumor cells down regulate stress markers and up regulate CD80/PD1; Ab binds; NK do their thing; Not MHC resitricted like CTL so anyones cells work; Receptor for Fc end of IgG
  • Ab’s; 1.) CD3 to bring CTL close 2.) Bind antigen receptor (presumably cancer); brings both together
  • Activate compliment, invoke ADCC, tagged with poison, radioisotope to kill cell
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5
Q

Immunodiagnosis:

  1. ) Serum protein electrophoresis: Measure what? Indirect test of? 5 peaks? Normal? IgA deficiency? Multiple myeloma? Pus infection? Hypogamma?
  2. ) Radial Immunodiffusion: Measures? Could also measure? (2) Size of circle tells you? Compared to?
  3. ) Mixed cyroglobulin test: Works how? Good for?
  4. ) RF test: Done how?
  5. ) ANA: Done how?
  6. ) Direct immuno test: Steps? (2)
  7. ) Indirect: Steps? (3)
A
  1. ) Globulin proteins in blood; humoral immune response; albumin, a1, a2, b, gamma globulins; small bump, can’t tell; single sharp peak; peaked gamma; low/no bump
  2. ) Individual globulin counts; compliment, clotting factors; how much IgA in blood (example); standard
  3. ) Immune complexes insuluble in cold; add to fridge; type 3 is suspected
  4. ) Latex particles coated with IgG then add IgM
  5. ) Permeable human cells then add pt’s serum
  6. ) Tissue on slide; add flourescent ab to know bacteria (checking for antigen)
  7. ) Bacteria on slide; add florescent ab’s; goat ab; test for presecene of antibody
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6
Q

Immunodiagnosis:

  1. ) ELISA steps? (3) Now used?
  2. ) Sandwhich ELISA? Steps? (3) Used to test? 2 MABs must have? Amount of color change?
  3. ) Passive agglutination: Measure what? Percipitation test? Passive test? Measures titer which is? No agglut? Agglut?
  4. ) Skin Test: Test for what? Read how long after?
  5. ) DTH Test: Done how? Test for?
  6. ) Steps to positive TB test? (6)
  7. ) Flow cycometry: Evaluates? Measured by adding? Then?
  8. ) T cell function measured how?
  9. ) Chest x ray?
  10. ) Lymphoid biopises to look at?
A
  1. ) Add ag to plate; add goat IgG with radioisotope; Mouse MAB with an enzyme
  2. ) Add Plate with 1 MAB; Add pt’s serum; Wash and add second MAB with enzyme; detect antigen; epitopes for antigen; amount of antigen
  3. ) Amount of a specific ab in pt’s serum; primitive, mix pt’s serum and Ag looking for ppt; more sensitive; ag is added to RBC/bead then add dilutions of pt’s serum; lowest amount of serum to make agglut; point; diffused
  4. ) TH1 via hypersensitivity; 24-48 hours
  5. ) Good test for T cells; paint on skin
  6. ) Ab endo by DC; Ag digested; Ag on Class 2 MHC; anti TB TH1 come by; Release IFNg; mac’s activated
  7. ) T cell #; MABs to CD3,CD4,CD8
  8. ) Add serum to mitogen and measure cytokines
  9. ) Examine size and presecense of thymus
  10. ) Markers
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7
Q

Tumors:

  • Immunosureilanve theory? Malignancy =? Evidence for? (3) Evidence against? (2)
  • Immunoediting: 3 stages and definitions?
  • Tumor associated antigen? 3 gene products? (ex)
  • Carcinoembryonic antigen? Often found it what patients? Kit example? But? Better use?
  • CTL cells role in cancer? Mediated by? (2)
  • NK role in cancer? 2 tricks? Supressed by?
A
  • Role of immune system (part. t cells) is to monitor cell surfaces and destroy abnormal cells; failed immune system; immunodeficient pt’s get cancer, presence of T cells on tumor is good sign; some tumors regress due to immune system; immunodef. pts get certain types of cancer; nude mice get few cancers
  • 1.) Elimination = malignant cells recognized and cleared
    2. ) Equilibrium = Tumor not destroyed but not growing
    3. ) Escape = Escapes surveilence via tricks
  • not found on normal cell, if recognized then destroyed; viral=HPV, EBV; mutant = chemical/physical carcinogenesis (often vary pt. to pt.); normal = oncofetal lineage
  • Oncofetal antigen; colon cancer; CEA; many false positives; use if suspicious or track progress
  • CD8’s recognize TAA via class 1; Fas mediated apoptosis or IFNgamma to bring in Macs
  • Don’t have to be from host; check for stress markers (innate); ADCC (adaptive); MHC class 1 T cells
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8
Q

Tumors:

  • Adoptive Cell Transfer Therapy: Use what? Steps? (4)
  • Hellstrom experiment: 3? Blocking T cell function? Possible blocking factors?
  • Treatment: 3 B cell methods? T cell method?
  • BCG treatment?
  • Problem with MABs? (3)
  • Nude mice with no immune system: Why no cancer?
A
  • Pt’s own immune response; Pt’s Tumor Infiltrating lymphos taken; expand in culture with IL2; excise some tumor; add TIL’s back
  • 1.) T cells regressing tumors added to melanoma = killed
    2. ) T cells progressing tumors added to melanoma = killed
    3. ) T cells with progressive serum added = not killed
  • something in serum; Ab’s shielding tumor
  • MAB’s to increase compliment/ADCC/ tagged with poision; MAB to decrease autocrine; AB with chain for CD3 and target marker…Activate RE system to clear blocking factors
  • Inject it into tumor; delayed hypersensitivity with innocent bystander (tumor)
  • Ab’s not best against tumors; cancer evolve to down reg certain epitopes; many false positives as screen
  • High NK cell
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9
Q

AIDS:

  • HIV seropositive means?
  • AIDS? (2)
  • Virus: Genes? Oncogene? Reproduce via? Contain? (7)
  • Orgin: When? Where? From? US when? Came via?
  • Epi: In US? Don’t know? Worldwide? Stabilized?
  • Pathogenesis: Blood virus peaks? Ab’s peak? Latency - average incubation? 10 steps? Initially infected cells cleared? But? CD4:CD8 goes from? To?
A
  • Have Ab to HIV

- CD4

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10
Q

AIDS:

  • Potential drug target? (4)
  • 32 BP deletion of CCR5: Need? Infected? Sick?
  • Elite controllers?
  • TH2/TfH in HIV patients? Ab’s? CTL’s?
  • Common infections: Primarily? (6) What’s fine?
  • Lab diagnosis algorithm: (4?)
  • Vaccine problems: Most vaccines stimulate? Problem with this? (2) HIV in general problems? (2) What may help?
A
  • CCR5, integrase, RT, protease
  • 2 mutated alleles; yes; CCR5 not expressed so not sick
  • HLA-B57 make great CTL response; harbor virus but don’t get sick (F/A pockets have high affinity for virus)
  • Prominant; not effective (hidden epitopes); not stimulated
  • T cell mediated ones; CMV, HSV, Candida, TB, Karposis; extra cellular bacteria response
  • OraQuick; ELISA to check Ab; Western for gp120/41; PCR
  • Ab response; epitopes hidden and evolving; high mutation rate with a high tolerance of mutations; mAB’s
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