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Immunopathology

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  • pg 1
									Section 3 Transplant Rejection
 1. Terms:
Autograft: transplantation within the same
  individual
Isograft or syngeneic graft: between identical
 twins or inbred animals
 Allograft: between individuals of the same species
 but of differing genetic make-up
 Xenograft: between different species.
           2. Types of rejection
(1) Superacute rejection:
①Time: within minutes or hours after transplantation.
②Causes: these are major incompatibility with high
 levels of humoral antibodies.
③Morphology:
 a. thrombotic occlusion of the capillaries
 b. Fibrinoid necrosis occurs in arterial walls.
 c. Infarction
 d. Neutrophils infiltrating
(2) Acute rejection

① Time:
Within days to weeks in the untreated
 recipient. Or may appear suddenly
 months or even years later, when
 immunosuppression      has      been
 employed.
② Types:
a. Acute cellular rejection: diffuse mononuclear
  cell infiltrating that may invade the tubules,
  causing focal tubular necrosis, and edema as
  well as mild interstitial hemorrhage.

b. Acute rejection vasculits (humoral rejection):
  necrotizing vasculitis with endothelial necrosis,
  neutrophils    infiltration,   deposition     of
  immunoglobulins, complement, and fibrin, and
  thrombosis the vascular intima is markedly
  thickened and inflamed.
             Schematic representation of the events
             that lead to the destruction of
             histoincompatible grafts. Donor class I
             and class Ⅱ antigens along with B7
             molecules are recognized by CD8+
             cytotoxic T cells and CD4+ helper T cells,
             respectively, of the host. The interaction
             of the CD4+ cells with peptides presented
             by class Ⅱ antigens leads to proliferation
             of TH1-type CD4+ cells and the release of
             interleukin 2 (IL-2) from the cells. IL-2
             further augments the proliferation of
             CD4+ cells generates a variety of other
             soluble mediators (lymphokines) that
             promote B-cell differentiation. The TH1
             cells also participate in the induction of a
             local delayed hypersensitivity reaction.
             Eventually, several mechanisms converge
             to destroy the grafe: (1) lysis of cells that
             bear class I antigens by CD8+ cytotoxic T
             cells, (2) antigraft antibodies produced by
             sensitized B cells, and (3) nonspecific
             damage inflicted by macrophages and
             other cells that accumulate as a result of
             the delayed hypersensitivity
             reaction.(From Robbins Basic Pathology
             ,2003)


Slide 7.20
   Acute cellular rejection of a renal allograft. A, An intense mononuclear cell
   infiltrate occupies the space between the glomerulus (bottom left) and the
   tubules. B, Tubule, highlighted by the basement membrane, undergoing
   destrction by invading lymphocytes. (Dr. Ihsan Housini)

    (From Robbins Basic Pathology ,2003)

Slide 7.21
    Antibody-mediated damage to the blood vessel in a renal allograft. The
    blood vessel is markedly thickened, and the lumen is obstructed by
    proliferating fibroblasts and foamy macrophages. (Dr. Ihsan Housini) .
    (From Robbins Basic Pathology ,2003)

Slide 7.22
       (3) Chronic rejection
① Time: months——years
② Morphology:
 Vascular changes consist of dense intimal
  fibrosis;
 Interstitial fibrosis, tubular atrophy,
  shrinkage of the renal parenchyma;
 Mononuclear cell infiltrates containing
  large numbers of plasma cell and
  numerous eosinophils.
(4) Graft-versus-host (GVH) disease:


It occurs in any situation in which
 immunologically component cells or
 their precursors are transplanted
 into immunologically crippled
 recipients.
3. Methods of increasing graft survival


(1) Favourable sites for transplantation
① cornea and anterior chamber of the eye
② meninges
③ testis
(2) Accurate tissue matching
(3) Immune deficiency states, pregnancy,
  and uraemia
(4) Immunosuppression
  ① Corticosteroids
  ② Azathioprine
  ③ Antilymphocyte serum
  ④ Whole-body irradiation
  ⑤ Induction of immune tolerance

								
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