sys5 notes-1

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  1. In adaptive immunity, what is the faster response?
    secondary because of memory. They learn antigen characterisitics
  2. why would receptors be able to change themselves?
    recognizze a large number of antiens via gene rearrangement.
  3. TCRs
    • alpha beta
    • gamma delta for musocal-5%
  4. BCRs
    hevay and light chains
  5. MHC restriction
    Ags must be presented to T-cells and B-cells in context of MHC complex
  6. where does autoimmunity come from?
    negative selection gone worong in thymus
  7. where do
    granulocytes come from
    • 1. lymphoid progenitor
    • 2. commonmyeloid progenitor
    • 3. common myelodi>myeloblast>monocyte>macrophage
    • 4. common myeloid progenitor>megakaryocyte>thromobocytes
  8. what kinds of t-cells are in the bone marrow?
    mostly memory t-cells. If bone marrow infected in trouble
  9. what are the cardinal signs of inflammation
    calor, dolor, rubor, tumor, increased permeability, adhesion, extravsation fo PMNs, macrophages
  10. what are antigen presenting cells that are activated
    dentritic cells, macrophages, B-cells( can be activated in t-cell dependent or independent manner)
  11. T-cell activation requires
    • MHC antigen presentation.
    • Co-stimulatory molecules B7-CD28
    • cytokiens
  12. cytokines role
    allow t-cells to be fully  activated and survive longer
  13. self reactive t-cells
    95% negatively selected for
  14. TCR development
    • None when first in thymus
    • they bithe CD4/CD8
    • then only one
  15. clonal selection
    when t-cells or b-cells are fully activation. central pricniple of adaptive immunity
  16. 2 signals for lymphocyte activation
    B-cells get Ag binding and T-cell activation
  17. role of antibodies
    neutralization, opsinization, activation of complment
  18. CD8 t cells in bacteria and virus
    MHC class I for virus or can see and directly kill bacteria

    cause lysis
  19. CD4 cytokines
    • Th1- INF-y and IL-2 inflammation macrophage
    • Th2- LI4,6,10 for B-cell activation
    • Th17- IL-17 acitvation of PMNs ORAL cavotu
    • T reg- inhibit overactivation of T-cells
  20. autoimmune patients can have problems in
  21. humoral vs cell mediated immunity
    extracellular vs intracellular
  22. primary lymhoid system
    • thymus
    • bone marrow
  23. secondary lymph system
    • lymph nodes
    • spleen
    • mucosal and cutaneous lymhoid tissues
  24. after infection what cells start migrating to lymph nodes
    macrophage and DCs
  25. epithelia barrier functions
    • skin and mucosa
    • musocal sites have specific antibodies(IgA) and mucin that prevents bacteria from sticking
  26. maturation of DCs
    DCs encounter PAM(some repetitive motif). Signaling cause DCs to move to lymph nodes
  27. activation of naive t-cells
    t-cells enter via HEVs
  28. whch t-cells inhibit immature DCs
  29. what do Th1s do?
    promote intracellular killing of bacteria in macriohages
  30. Th2s
    drive B-cells to differentiate and drives B-cells to produce antibodies
  31. naive b-cells
    • need helper t-cells
    • first have IgM then class switch
  32. affinity maturation
    specific for an Ag so its produces more of a receptor
  33. what causes class switching
    function dependent, particular pathogens and cytokines drive the diff isoforms
  34. completion of immune response drives
    memory and then immune sys goes to basal state
  35. persisitnet pathogens
    herpes, can persist by ceasing to replication until immunty wanes, resist descruction.

    inappropriate immune response can lead to persisient disease
  36. tuberculosis
    virus escapes phagosome.
  37. immune dictates outcomes
    • leprosy( tuberculoid vs lepromatous leprosy)
    • tuberculoid Th1 response,
    • lepromatous generates Th2 response
  38. inappropriate immune response
    • hypersensitive
    • decfective immune system
    • gene defects
    • autoimmunity
  39. hypersensitivity
    • reaction against NONinfectious antigen.
    • IgG or IgE
    • susceptibility genes
  40. allergic reaction
    Th2 type primming
  41. immunodeficiency disease
    primary due to mutations in genes that are important in controlling response.
  42. autoimmunity
    due to failure of intrinsic tolerance mechanism
  43. ex type I diabetes
    effector t-cells start recognizing and start killing beta cells
  44. hypersenitivity typically involve
    IgG, IgE, or specific t-cells
  45. type I hypersensitivity
    allergies, and anaphylactic type mediated by IgE mass cells and basophils
  46. Type II
    antibody dependent, directed against antibody to fixed tissue
  47. Type III
    like type II but response against soluble antigen
  48. Type IV
    T-cell mediated, sensitived T-cells, graft rejection, asthma, contact dermatitis
  49. effector mechanism of type I
    • mast cell activation to produce IgE:
    • allergen crosslinks
  50. initial Type I
    release of vasoactive amines (histamine) from basophils and mast cells
  51. late Type I
    the involve recruitment of inflammatory cells and damage
  52. Role of IgE
    • IgE binds to mast cell to Fc. Acivates mast cells.
    • Amount and location of allergen
  53. activating mast cells
    • reside near mucosal surfaces.
    • binding of Ag-Ab-FcR on mast cell triggers a granule to relelase its contents
  54. histamine
    • increased vascular permeability
    • vasodilation
    • mucus production
    • bronchorestriction
  55. Trigger from mast cell
    proteases-tryptase kinins and complement components

    chemtactic ffactors for recruitment of neutrophil and eosininophil
  56. allergic reaction late phase response due to
    • prostaglandin, leukotrienes, histamine, etc.
    • cytokines (mast cells secrete TNF-a, IL-1, Il-4,6,5,)

    • some of these signals lead to b-cell switching
    • and activate PhosA2 to AAcid
  57. cleave of AAcid
    augments secondary response
  58. PAF platlet activating factor
    • augments inflame response
    • vasocontriction
    • broncocontriction
  59. cell-mediated immunity
    • intracellular pathogens (T-cells)
    • CD8
    • CD4Th1- macrophages
    • CD4Th2-class switching
  60. Humoral
    • extracellular microbes and toxins,
    • B-cell
  61. primary lymph organs
    bone marrow and thymus
  62. what triggers adaptive immunity
    migrating DCs and marophages to lymphnodes
  63. epithelia pathways
    epithelia activate pathways to inflammation and recruitment
  64. affinity maturation
    with repeated exposures, a host will produce antibodies of greater affinity(somatic hypermuation and clonal selection)
  65. IgE not good at
    neutralization or opsinization
  66. type I diabetes
    Type IV hypersensitivity reaction
  67. susceptible genes in hypersensitivity
    HLA and MHC
  68. Hypersensitivity reactions involve which antibodies
    IgG or specific T-cells
  69. Type I
    • anaphylactic, allergy IgE, Th2 activate class switching
    • IgE-Ag-mast cell binding
  70. Type II
    Ab dependent to fixed tissue
  71. Type III
    immune complex
  72. TypeIV
    cell-mediated, delayed
  73. Type I initial response/late
    • 5-30 minutes, basophils and mast cells
    • late recruitment of inflamm cells and epithelial damamge

    • degranulation>histamne
    • late phse>cytokines> TNF-alpha, IL-1,4,5,6, leukotrienes and prostaglandins
  74. AA via lipoxygenase and cyclooxgenase
    leukotriene and prostaglandin
  75. rhinitis, hives, urticaria
    type I,

    complement cause cause granule release
  76. atopic asthma
    initital binding to basement membrane, membrane thickeding, edema, increase in gland sixe and hypertrophy of branchial muscle walls
  77. systemic anaphylasis in minutes with layrngeal edema branochoconstriciton

    BUT anaphylactiv shock is
    systemic vasodilation
  78. testing for IgE sensitivity
  79. Type II-goodpasture, penicillin
    IgG An direct cell surface binding
  80. Type II diseases
    • Graves (AB mediated stimulation
    • drug
  81. GOodpasture
    • AB against basment membrane in kidney and lung (teens-20s, male)
    • glomernephrisits and intersitital pnemonia
  82. mechanisms for AB mediated injury
    • complment dependent rxns
    • AB mediated cellular dysfunction
    • -direct cell lysis or opsination and phago
  83. pemphigus vularis
    Ab against desmosomal proteins lead to complement. Blisters  and lesions in oral and genital mucosa IgG
  84. Bullous pemphigoid
    blisters form do not rupture, elderly, IgG hemidesmosomes
  85. some do not cause inflmmaiton directly
    • myasthenia gravis block Ach receptor sites
    • Graves
  86. types of AB-meditated mechanisms in Type II
    • opsinization
    • complement/inflamm
    • cell dysfunction
  87. Opsinization in type II
    • cells from incompatible donor are opsinized (hemolytic disease of newborn diff igGs b/t mother and fetus)
    • thrombocytopenia...Abs to own RBCs
  88. Tyoe II complement mediated
    • Goodpastures
    • Pemphigus vulgaris
  89. Type II celluar dysfunction
    myastenia gravis, Graves
  90. Type III vs Type II
    III against a soluble antigen via Immune complex
  91. immune complex is deposiited throught the body
    • leading to complement activation and PMN actvity 
    • symptoms: fever, rash, arthritis, glomernephritis
  92. immune complexes are not tissue specific found in
    small vessels, joints, kidnet, heart
  93. Type III characterisitics
    PMN infiltrate, nectrotizing tissue, vasculitis
  94. TYPE III examples( can be with self or exogenous)
    • serum sickness, strep glomerlonephritis, 
    • chronic exposure- lupus
    • local complex- arthus only skin necrosis
  95. serum sickness upon foreign serum injection
    Ag-AB complex, and AB in plasma shoots up
    fever vasculitis, arthitis, nephritis
  96. poststreptococcla glmerunephrtis
    type III
Card Set:
sys5 notes-1
2013-08-07 16:00:58
sys5 notes

sys5 notes
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