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Pathology - Acute Rejection of Transplant
Acute rejection of transplanted kidney, the most prevalent type of transplant rejection.
The patient will present with indicators of rejection anywhere from days to up to 6 months post-transplant, which may include myalgias, arthralgias, fever, chills, or other organ-related symptoms such as oliguria for a renal transplant. However, organ-specific function laboratory tests may be the only indication that rejection is occurring, requiring constant monitoring of transplant recipients. The mechanism of acute rejection is a type IV cell-mediated hypersensitivity and concurrent type II antibody-mediated hypersensitivity reaction. Although MHC antigen reactivity was screened for in HLA-matching, HLA complex minor histocompatibility antigens on the allograft (speciesspecific transplant) trigger CD4 + T cells in the recipient to produce cytokines and generate adhesion molecules. This results in proliferation and activation of CD8 + T cells, which release perforins leading to cell death, as well as stimulation of host macrophages by IFN-γ. Adhesion molecules facilitate lymphocyte movement, creating graft edema and endothelial cell damage. The autoantibody reaction is driven by B cell development into plasma cells, producing anti-HLA antibodies, resulting to vasculitis or intimal thickening of the graft. Acute rejection can be controlled with immunosuppressive treatment and is generally reversible. Decline in organ function, which happens many months to years after transplant is chronic rejection. Its mechanism is not well known but results in ischemia to tissue and may be a result of repeated episodes of acute rejection.
Acute rejection of transplanted kidney, the most prevalent type of transplant rejection.
The patient will present with indicators of rejection anywhere from days to up to 6 months post-transplant, which may include myalgias, arthralgias, fever, chills, or other organ-related symptoms such as oliguria for a renal transplant. However, organ-specific function laboratory tests may be the only indication that rejection is occurring, requiring constant monitoring of transplant recipients. The mechanism of acute rejection is a type IV cell-mediated hypersensitivity and concurrent type II antibody-mediated hypersensitivity reaction. Although MHC antigen reactivity was screened for in HLA-matching, HLA complex minor histocompatibility antigens on the allograft (speciesspecific transplant) trigger CD4 + T cells in the recipient to produce cytokines and generate adhesion molecules. This results in proliferation and activation of CD8 + T cells, which release perforins leading to cell death, as well as stimulation of host macrophages by IFN-γ. Adhesion molecules facilitate lymphocyte movement, creating graft edema and endothelial cell damage. The autoantibody reaction is driven by B cell development into plasma cells, producing anti-HLA antibodies, resulting to vasculitis or intimal thickening of the graft. Acute rejection can be controlled with immunosuppressive treatment and is generally reversible. Decline in organ function, which happens many months to years after transplant is chronic rejection. Its mechanism is not well known but results in ischemia to tissue and may be a result of repeated episodes of acute rejection.
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