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immunopathy Flashcards

1
Q

Type I

A
  • immediate hypersensitivity the injury is caused by TH2 cells, IgE antibodies, and mast cells and other leukocytes
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2
Q

type II

A
  • Antibody-mediated disorders, secreted IgG and IgM antibodies injure cells by promoting their phagocytosis or lysis and injure tissues by inducing inflammation
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3
Q

type III

A
  • immune complex-mediated disorders, IgG and IgM antibodies bind antigens usually in the circulation, and the antigen-antibody complexes deposit in tissues and induce inflammation
  • Ex: systemic lupus erythematosus = nuclear antigens
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4
Q

type IV

A
  • in cell-mediated immune disorders, sensitized T lymphocytes (TH1 and TH17 cells and CTLs) are the cause of the tissue injury
  • Ex: Rheumatoid arthritis = inflammation mediated by Th17 cytokines
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5
Q

autograft

A
  • tissue grafted from one bodily site to another on the same individual
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6
Q

isograft

A
  • tissue grafted between identical twins
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7
Q

allograft

A
  • tissue grafted from one individual to a genetically different individual of same species
  • from cadaver or living donors
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8
Q

Xenograft (heterologous)

A
  • tissue grafted between species; rare, pig heart valves are an example
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9
Q

describe KIDNEY: Cell-mediated cytotoxicity

A
  • Type IV hypersensitivity rxn
  • cell-mediated, occurs because the donors’ graft elicits a CTL reaction to destroy the graft;
  • -> donor APC stimulates the recipient’s CTLs
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10
Q

describe KIDNEY: delayed type hypersensitivity

A
  • Type IV hypersensitivity rxn
  • delayed-type, TH cells secrete cytokines, which results in inflammatory mediator release and tissue damage;
  • -> recipient APCs take up Ag from the graft
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11
Q

describe KIDNEY: humoral mechanisms

A
  • Target graft vasculature
  • -> Ab bind to HLA molecules in graft endothelium, activate complement –> acute inflammation or vasculitis resembling type II hypersensitivity reaction
  • -> Ag-Ab complexes form in circulation or in situ (type III), fix complement –> necrotizing, immune complex vasculitis
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12
Q

describe KIDNEY: hyperacute rejection

A
  • recipient sensitized by prior transplant, multiple transfusions or pregnancies
  • preformed Ab react against Ag in allograft endothelium –> local immune complex formation (III), complement activation, vasculitis with fibrinoid necrosis, thrombosis, ischemia
  • immediate or within minutes to hours
  • avoided by cross-matching recipient serum with donor lymphocytes to determine presence of cytotoxic Ab to donor MHC Class I and II antigens
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13
Q

describe KIDNEY: acute rejection

A
  • progresses rapidly once initiated
  • mediated by cellular, humoral or combined/overlapping mechanisms
  • occurs days-months post transplant or after withdrawal of immunosuppressive therapy
  • LOTS OF INFLAMMATION!!
  • Destroys epithelial cells and vessels
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14
Q

KIDNEY: acute cellular rejection

A
  • Cytotoxic (CD8+) lymphocytes infiltrate tubular & vascular basement membranes –> tubular damage, endothelitis
  • Helper T-cells (CD4+) produce cytokines –> extensive interstitial inflammation
  • typical morphology: lymphocytic infiltrates and tubular necrosis
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15
Q

KIDNEY: acute humoral rejection

A
  • anti-graft Ab deposit in graft vasculature
  • morphologic patterns:
  • -> necrotizing vasculitis
  • -> intimal thickening due to accumulation of fibroblasts, foamy macrophages, myocytes
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16
Q

KIDNEY: Chronic rejection

A
  • occurs months to years after transplantation possibly from repeated humoral or cellular insult
  • possible mechanisms:
  • -> humoral injury = proliferative vascular lesions
  • -> cellular injury = cytokine induced proliferation of vascular smooth muscle and production of COLLAGEN in ECM
  • Morphology: vascular changes, interstitial FIBROSIS, tubular atrophy, chronic inflammation
17
Q

Liver transplantation

A
  • Tx for progressive, advanced liver disease with organ failure; most common indication is Hepatitis C
  • second most common solid organ transplanted
  • Size, ABO grouping important, lesser requirement for immunosuppression than other solid organs
18
Q

Acute Liver Rejection

A
  • cellular reaction occurs within 3 months following transplantation
  • mixed inflammatory cell infiltrates with eosinophils
  • infiltrate of lymphocytes, plasma cells, macrophages expanding portal tract causing damage to bile ducts
  • Triad of features
  • -> portal tract inflammation
  • -> bile duct epithelial damage
  • -> endothelitis of portal vein and hepatic artery branches
19
Q

Chronic liver rejection

A
  • progressive disappearance of bile ducts due to direct immunologic destruction or loss of blood supply
  • More Jaundice (AST and ALT are up)
  • obliterative arteritis from proliferation of intimal layer –> ischemic changes
  • End result = portal and hepatic fibrosis
20
Q

Heart transplantation

A
  • treatment for advanced, irreversible myocardial disease with intractable congestive heart failure (cardiomyopathy)
  • classic cellular rejection with interstitial and perivascular T cell infiltrates –> myocyte necrosis that histologically resembles myocarditis
  • major complication: diffuse intimal proliferation –> coronary artery disease
21
Q

acute cardiac rejection

A
  • endomyocardial biopsy showing lymphocytes surrounding and destroying myocytes
22
Q

chronic cardiac rejection

A
  • coronary artery showing intimal proliferation with chronic inflammation
  • transplantation associated arteriopathy
23
Q

cyclosporine

A
  • blocks nuclear factor of activated T cells (NFAT), a transcription factor necessary for IL-2 stimulation of T cells
24
Q

steroids

A
  • supress macrophage activity and inflammation
25
Q

azathioprine

A
  • inhibits DNA synthesis
26
Q

Graft v host disease

A
  • cell mediated reaction: donor T cells recognize the Host HLA antigens as foreign and mount a Type IV (DTH or CTL) reaction against graft elements and tissues
  • immunocompetent graft cells destroy immunocompromised recipient cells
27
Q

Acute GVHD

A
  • Occurs days-weeks post engraftment
  • mechanisms: donor cytotoxic T cells or cytokines from helper T-cells destroy epithelial cells
  • leads to:
  • -> skin changes = rash, exfoliation
  • -> GIT changes = ulcerative gastroenteritis
  • -> hepatic changes = bile duct necrosis
  • profound immunosuppression –> susceptibility to infection
28
Q

Chronic GVHD

A
  • follows resolution of acute GVHD but may evolve insidiously without apparent acute phase
  • develops from autoreactive T cells derived from donor stem cells that cannot be clonally deleted due to minimal immune function of recipient
  • morphology mimics systemic sclerosis with generalized fibrosis
29
Q

transplantation of hematopoietic cells

A
  • Treatment for hematologic disorders, non-hematologic malignancies, immunodeficiencies
  • Stem cells harvested from donor bone marrow or from peripheral blood following simulation by hematopoietic growth factors
  • Complications = graft versus host disease, infection, immunodeficiency

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