giovanni83
Forum Senior
Topics: 24
Posts: 125
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Hi guys, I want to make clear this point:
TRANSPLANT REJECTION:
I know that initially there's a type 2 hypersensitivity reaction, and then can occurs a type 4 hypersensitivity reaction caused by presensitized fagocities...
My question is: what are the steps of reaction? (ex.:1 week: Ig; 1 month: PMN; 1 year: ....) and in which of this steps are there hypersensistivity reactions?
Thanks to all...
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| young_doc
Forum Guru
Topics: 56
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Hyperacute, within minutes: pre-formed anti-donor Ab's. Type 2.
Acute, within weeks: Cytotoxic T-cell mediated (reversible with immunosuppression). type 4.
Chronic, months to years: Ab-mediated vascular damage, irreversible (fibrinoid necrosis). Not sure if this one is hypersensitivity or not...or if it is, not sure whether it's Type 2 or 3?
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| giovanni83
Forum Senior
Topics: 24
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thanks very much, now all is clear 4 me...
ps:I don't know if the cronic reaction is type 2 or 3...
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my msn messenger address is squadracalcetto@interfree.it ; my email address is giovanni83@email.it ; and my website is http://www.appuntimedicina.it ciao ciao
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| ManuNastai
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Don't know about the cronic one, but vascular damage is done by deposition of immune complexes in the vascular wall which activate complement, C3b atracts neutrophils which destroy the vessels. This is a type III hypersensitivity reaction.
Remember a hypersensitivity reaction occurs when there is a immune response that produces damage to the organism in one way or another.
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| Musuq
Forum Guru
Topics: 103
Posts: 425
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IMMUNOLOGY OF TRANSPLANTATION
Rejection
Hyperacute rejection
Acute rejection
Chronic rejection
In clinical transplantation, three main types of rejection may occur: hyperacute, acute, and chronic. Regardless of the type of rejection, warning signs include fever, flulike symptoms, hypertension, edema or sudden weight gain, changes in heart rate, shortness of breath, [and pain and tenderness over the graft site].
Hyperacute rejection
Occurring within minutes to days of transplantation, hyperacute rejection is due to preformed IgG antibodies in the recipient that react against class I HLA in the transplanted organ. Organ function is lost as a result of antibody deposition, complement activation, and vascular destruction. Kidney transplants are most susceptible to hyperacute rejection. However, hyperacute rejection can be prevented by detecting the antibody with simple cross-matching prior to transplantation, and it is now rare.
Acute rejection
The most common form, acute rejection occurs most frequently in the first 6 months after transplantation. After 6 months, the body adapts to the new organ, and acute rejection is less likely. Acute rejection is mediated by T cells, which infiltrate the allograft, undergo clonal expansion, and cause tissue destruction. Immunosuppressive drugs are most effective in preventing this type of rejection.
Chronic rejection
Chronic rejection is the term used when allograft function slowly deteriorates and there is histologic evidence of intimal hypertrophy and fibrosis. Chronic rejection can occur in all types of organ transplants. In heart transplants, it manifests as progressive coronary artery disease; in lung transplants, as bronchiolitis obliterans; and in kidney transplants, as progressive interstitial fibrosis, tubular atrophy, and glomerular ischemia. The liver appears to be less affected by chronic rejection, but when it does occur, biliary epithelium is lost, eventually leading to hyperbilirubinemia and graft failure.
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