Immunology Flashcards
1
Q
Immunohematology:
- ) A Blood: Possible genotype? RBC Antigen? Ab’s in plasma? Can donate? Receive? Common?
- ) B Blood: Possible genotype? RBC Antigen? Ab’s in plasma? Can donate? Receive? Common?
- ) AB Blood: Possible genotype? RBC Antigen? Ab’s in plasma? Can donate? Receive? Common?
- ) 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
- ) AA, AO; A; Anti B; A & AB; A & O; 42%W,27%B
- ) BB, BO; B; Anti A; B & AB; B & O; 9%W, 21%B
- ) AB; A, B; None; ABonly; A,B,AB, O; 3%W; 4%B
- ) 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
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)
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
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
5
Q
Immunodiagnosis:
- ) Serum protein electrophoresis: Measure what? Indirect test of? 5 peaks? Normal? IgA deficiency? Multiple myeloma? Pus infection? Hypogamma?
- ) Radial Immunodiffusion: Measures? Could also measure? (2) Size of circle tells you? Compared to?
- ) Mixed cyroglobulin test: Works how? Good for?
- ) RF test: Done how?
- ) ANA: Done how?
- ) Direct immuno test: Steps? (2)
- ) Indirect: Steps? (3)
A
- ) 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
- ) Individual globulin counts; compliment, clotting factors; how much IgA in blood (example); standard
- ) Immune complexes insuluble in cold; add to fridge; type 3 is suspected
- ) Latex particles coated with IgG then add IgM
- ) Permeable human cells then add pt’s serum
- ) Tissue on slide; add flourescent ab to know bacteria (checking for antigen)
- ) Bacteria on slide; add florescent ab’s; goat ab; test for presecene of antibody
6
Q
Immunodiagnosis:
- ) ELISA steps? (3) Now used?
- ) Sandwhich ELISA? Steps? (3) Used to test? 2 MABs must have? Amount of color change?
- ) Passive agglutination: Measure what? Percipitation test? Passive test? Measures titer which is? No agglut? Agglut?
- ) Skin Test: Test for what? Read how long after?
- ) DTH Test: Done how? Test for?
- ) Steps to positive TB test? (6)
- ) Flow cycometry: Evaluates? Measured by adding? Then?
- ) T cell function measured how?
- ) Chest x ray?
- ) Lymphoid biopises to look at?
A
- ) Add ag to plate; add goat IgG with radioisotope; Mouse MAB with an enzyme
- ) Add Plate with 1 MAB; Add pt’s serum; Wash and add second MAB with enzyme; detect antigen; epitopes for antigen; amount of antigen
- ) 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
- ) TH1 via hypersensitivity; 24-48 hours
- ) Good test for T cells; paint on skin
- ) Ab endo by DC; Ag digested; Ag on Class 2 MHC; anti TB TH1 come by; Release IFNg; mac’s activated
- ) T cell #; MABs to CD3,CD4,CD8
- ) Add serum to mitogen and measure cytokines
- ) Examine size and presecense of thymus
- ) Markers
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
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
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
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