shosh: immmuno

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shosh: immmuno
2011-08-02 18:19:59

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  1. What does the thoracic duct drain into?
    Left subclavian
  2. Positive T cell selection
    • Selects for T cells that can bind MHC
    • Occurs in cortex of thymus
  3. Negative T cell selection
    • Selects for autoreactive T cells
    • Occurs in medulla of thymus
  4. Where are small antigenic peptides attached to MHC I?
  5. What is significant about CD5+ B cells?
    They have not undergone class switching, and can only produce IgM
  6. Function of perforin and granzymes
    • Perforin delivers NK cell granule contents into infected cells
    • Granzyme activates serine proteases, which triggers apoptosis
  7. What activates T helper cells?
    Foreign antigen presentation on MHC II, with help of B7 costimulatory molecule
  8. Which MHC activates cytotoxic T cells?
    MHC I (presents viral or self antigens)
  9. Where is the CD40 ligand located, and what does it do?
    • CD 40 ligand on T helper cell membrane
    • Mediates AB class switching
  10. Function of immunoglobulins alpha and beta on B cell membrane
    Transduce AG binding signal to cytoplasm
  11. Difference between pro-B cells and pre-B cells
    • Heavy chain rearrangement occurs in pro-B cells
    • Light chain rearrangement occurs in pre-B cells
  12. tDt
    • Randomly inserts nucleotides between D and J regions during DNA synthesis to increase affinity of AB for AG
    • Used as a marker for ALL
  13. Which antibody does not undergo somatic hypermutation?
  14. What is a thymus independent antigen?
    Thymus independent antigens lack a peptide component, so cannot be presented by MHC to T cells. They stimulate release of IgM only, and do not activate memory
  15. EBV receptor
    CD21, found on B cells
  16. Primary opsonins
    C3b and IgG
  17. C3 deficiency
    • Recurrent pyogenic and respiratory infections
    • Increased susceptibility to type III hypersensitivity reactions
  18. DAF deficiency
    DAF helps prevent complement activation against self-cells. Is deficient in PNH.
  19. How do interferons kill viruses?
    They induce production of a ribonuclease that degrades viral mRNA
  20. What type hypersensitivity reaction are serum sickness and arthus reaction?
    • Type III
    • Present with fever, urticaria, and arthralgias, 5--10 days after antigen exposure
  21. Hypersensitivity reactions: Grave's and Hashimoto's
    • Graves--type II
    • Hashimoto's--type IV
  22. What are the type IV hypersensitivity reactions?
    • Diabetes I
    • Celiac
    • Guilliane-Barre
    • Hashimoto's
    • MS
    • GVHD
    • PPD
    • Contact dermatitis
  23. 6 month old boy presents with recurrent bacterial infections, decreased B cells, and decreased immunoglobulins
    • Bruton's agammaglobulinemia
    • Defect in BTK tyrosine kinase gene
    • XR
    • B cell maturation is impaired
  24. Baby presents with severe pyogenic infections and increased IgM with no other immunoglobulins
    • HyperIgM
    • Caused by defective CD40 ligand on T helper cells
  25. Patient with a history of respiratory infections experience anaphylaxis after a blood transfusion
    • Selective Ig deficiency, due to defective class switching
    • Most common is IgA deficiency
    • Patients often develop antibodies against the missing Ig--so don't transfuse!
  26. Which Ig do Di George patients have?
    IgM only, since T cells are needed for class switching
  27. Patient has recurrent disseminated mycobacterial infections and low interferon gamma
    • IL12 receptor deficiency
    • (IL12 is secreted by macrophages and activates T helper 1 cells)
  28. Patient presents with staphylococcal abscesses, retained primary teeth, eczema, and increased IgE
    • HyperIgE/Job's syndrome
    • T helper cells cannot produce interferon gamma, which inhibits neutrophil response to chemotactic stimuli
    • Normally, IFN gamma inhibits T helper 2 cells--too many T helper 2 cells results in elevated IgE
  29. Primary defense against cutaneous and hematogenous candida infection
    • T cells protect against cutaneous candida
    • Neutrophils protect against disseminated candida
  30. Name 3 causes of SCID
    • Defective IL2 receptor (X linked)
    • Adenosine deaminase deficiency
    • Missense mutation in RAG
  31. Patient presents with TTP, recurrent infection, and truncal eczema.
    • Wiskott-Aldrich
    • Progressive B and T cell deletion, due to an XR mutation in cytoskeleton proteins
  32. Patient presents with cerebellar ataxia, spider angiomas, and IgA deficiency
    Ataxia telangiectasia, caused by defective DNA repair enzymes
  33. A baby presents with recurrent bacterial infections and delayed separation of umbilicus
    • LAD
    • Defective integrin protein on phagocytes impair ability of leukocytes to adhere to endothelium
  34. Patient presents with recurrent staph and strep infections, pale skin, and peripheral neuropathy
    • Chediak-Higashi
    • An AR defect in microtubule function impairs phagocytosis
  35. Patient presents with a history of recurrent infections by catalase positive organisms (staph, E. coli, aspergillus)
    Addition of nitroblue tetrazolium to blood sample does not make sample turn blue
    • CGD
    • Due to lack of NADPH oxidase
  36. Mechanism and side effect of cyclosporine
    • Inhibits calcineurin, which prevents release of IL2, thereby blocking T cell activation
    • Major side effect is nephrotoxicity, which can be controlled with mannitol diuresis
  37. Mechanism and side effects of tacrolimus
    • Binds to FK binding protein and inhibits IL2 release
    • Causes nephrotoxicity, peripheral neuropathy, and hyperglycemia
  38. Muromonab
    Monoclonal antibody against CD3, inhibits T cell signal transduction
  39. Sirolimus (rapamycin)
    • Binds to MTOR, inhibits T cell proliferation in response to IL2
    • Causes hyperlipidemia
  40. Mycophenolate mofetil (MMP)
    Inhibits de novo guanine synthesis
  41. Daclizumab/Basiliximab
    Monoclonal antibody against IL2 receptor
  42. What is oprelvekin used for?