type 3-4 HS

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ghrelin23187
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229317
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type 3-4 HS
Updated:
2013-08-06 13:53:37
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HS
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  1. what's the different between type 2 and 3 HS?
    both are antibody-mediated but Type 3 is against soluble antigen in the blood vs antigen bind to basement membrane or non-blood area
  2. mechanism of AB-mediated injury in type 2
    opsonization (complement dependent)

    • Fc-mediated on the leukocyte --> initiate inflammation (fix tissue, basement membrane) 
    • Inc production of C3a-C5a --> inc vasodilation and recruitment of PMN and immune cells 

    AB-mediated by binding to the receptor --> can both activate and inactivate the receptor (Myasthenia gravis and Grave disease)
  3. steps involve in type II HS
    1.Deposition of Immune Complexes

    • Antigen-antibody complexes produce tissue
    • damage by eliciting inflammation at site of deposition

    • Antigens:  exogenous (foreign protein)
    •             endogenous (self-component)
    • -get circulating immune complexes
    • that can be deposited in many organs or localized to one.

    2.Complement Activation

    3.Neutrophil Accumulation
  4. 3 phases of systemic type III HS
    • 1.Introduction of antigen triggers an immune response that produces antibodies.  (Takes about a week)
    •      Antibodies are secreted into blood where
    • they react with antigen still present in circulation, forming an antibody-antigen complex.

    2.Next phase:  Deposition of immune complex

    Circulating Ab-Ag complexes are deposited in various tissue. 

    • What determines whether complex formation will lead to tissue deposition and
    • disease?

    1.Complexes that are medium size

    2.Formed in slight antigen excess

    • 3.Tissue Injury caused by immune
    • complex:  Once in tissue, complexes
    • initiate acute inflammatory response.
  5. clinical features of Type III
    Fever

    Rash/Urticaria (hives)

    Arthritis

    glomerulonnephritis
  6. Type III: Immune complex found in
    Small blood vessels

    Joints

    Kidney

    Heart
  7. Distinguishing characteristics Type III Hypersensitivity
    •Intense neutrophilic infiltration

    • •Necrotic tissue will have deposits of
    • immune complexes (called fibrinoid necrosis)

    •Acute necrotizing vascularitis (necrosis of the vessel wall)
  8. Examples of Type III hypersensitivity
    • I.Single large exposure to antigen 
    • Usually resolves
    • •acute serum sickness
    • •Streptococcal glomerulonephritis

    • II. Chronic exposure to antigen
    • •Systemic lupus erythematosus
    • •Streptococcal glomerulonephritis

    • III. Local immune complex disease (Arthus
    • reaction)
    • •Usually in skin
    • •Reproduced by injecting antigen in
    • an immunized animal
  9. serum sickness
    take time to form complex --> deposit lead to fever vasculitis arthritis and nephritis 

    delayed in response of inflammation
  10. Poststreptococcal Glomerulonephritis
    •Most common in children 6-10 years old after a streptococcal infection

    •Antibody to streptococcal ag form compounds that deposit in glomeruli.

    vasculitis and intense neutrophil reponse 

    repeat and prolong exposure --> lupus
  11. Arthus rxn
    local immune complex disease 

    Localize area of tissue necrosis resulting from acute immune complex vasculitis

     take 1-2 hours
  12. Type IV Hypersensitivity - 3 effector mechanism
    • 1.Macrophage activation by TH1 cells, which
    • results in an inflammatory response.

    • 2.Damage is caused by activation of TH2
    • cells.  Inflammatory response is predominated by eosinophils

    • 3.Damage is caused directly by cytotoxic T
    • cells (CTL).
  13. whicchc type IV HS is predominated by eosinophil
    Th2 mediated
  14. Type IV Hypersensitivity Responses
    •Reactions are mediated by T cells

    •All take some time to develop (delayed 

    • •3 syndromes, grouped according to
    • the route by which antigen passes into body. 
    • Injected into the skin
    • abosorbed into skin
    • Aborbed by gut
  15. Type IV hypersensitivity - 3 stages
    Take 24-72 hours

    • 1st phase: uptake, processing and presentation of the antigen by local antigen
    • presenting cells

    • 2nd phase: TH1 cells that were primed by a previous exposure to the antigen migrate
    • into the site of injection and become activated.  Because these specific cells are rare, and
    • because there is little inflammation to attract cells into the site, it can
    • take several hours for a T cell of the correct specificity to arrive.

    • 3.  These cells release mediators that activate local endothelial cells, recruiting an inflammatory cell infiltrate dominated
    • by macrophages and causing the accumulation of fluid and protein.  At this point, the lesion is apparent.
  16. Elicitation of Type IV (delayed) hypersensitivity
    • 1.A contact sensitizing agent is a small
    • highly reactive molecule that can easily penetrate intact skin.  It binds to a variety of endogenous proteins, which are taken up and processed by Langerhan cells (major antigen presenting cell of the skin)

    • 2.These APCs present the peptides to
    • effector (and previously primed) TH1 cells

    3.Activated TH1 cells secrete IFN-g that then activate kerintocytes to secrete more cytokines and chemokines.

    • 4.These products recruit and activate
    • macrophages resulting in an inflammatory lesion.
  17. IFN-G activate
    macrophage
  18. Mechanism of T cell mediated HS
    • Delayed type HS and immune inflammation:
    • Th1 (macrophage) and Th17 (neutrophil)
    • --> depend mostly on cytokine secreted. TH17 at the lesser extense
    • Tcell-mediate: CLT --> kill
  19. Delayed Hypersensitivity (DTH) rxn (what test?_
    1.Injection of tuberculin in sensitized individual

    2.Local T cell inflammatory reaction

    3.Peaks at 24-72 hrs

    • Perivasular cuffing
    • Driven by T-cell secreted cytokines:IFNg, IL-12, IL-2, TNFa & lymphotoxin
  20. special form of DTH
    • granuloma 
    • lymphocyte on theh outside
    • epitheliod cell on the inside w/ giant cell
  21. rxn of CD*+ Tcells
    cell-mediated cytotoicity --> graft rejection and
  22. 2 mechanism for rejection of allograft
    direct and indirect recognition
  23. T-cell Mediated Graft Rejection - direct allorecognition
    Host T cells (transplant recipient) are activated by APC within the transplanted tissue (graft).

    Host T cell activated by Graft APC
  24. T-cell Mediated Graft Rejection - -Indirect
    Allorecognition
    APC from the host present graft antigens to host T lymphocytes --> chronic rejection to graft

    • mediated by CD4 Tcell --> macrophage
    • and AB mediated
  25. between direct and indirect pathwya for graft rejection
    direct pathway
  26. 3 type of graft rejection
    hyperacute rejection

    acute rejection

    chronic rejection
  27. graft vs host disease
    when immunologically competent cells are transplanted into immunologically criplled recipient

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