Transplant rejection
Also known as: graft rejection, allograft rejection
Transplant rejection is the recipient's immune response against a transplanted organ or tissue, triggered by donor antigens the immune system recognizes as foreign. It is classified as hyperacute, acute, or chronic based on timing and mechanism.
Rejection happens because the immune system reads donor human leukocyte antigens (HLA) and ABO blood group antigens as non-self. Risk depends on the graft type: an autograft (tissue moved within one person) and an isograft (between identical twins) carry no rejection risk, an allograft (between genetically different members of the same species) is the usual clinical scenario, and a xenograft (across species) provokes the strongest response. HLA matching and lifelong immunosuppression are the two main tools for preventing rejection.
Hyperacute rejection occurs within minutes to hours. Preformed recipient antibodies against donor ABO or HLA antigens bind graft endothelium, activate complement, and cause widespread thrombosis and ischemic necrosis — a type II hypersensitivity reaction. The graft must be removed. Pre-transplant crossmatching is designed to prevent it. Acute rejection develops over weeks to months and is predominantly T cell–mediated, with a lymphocytic infiltrate and vasculitis on biopsy; an antibody-mediated form also exists. It often responds to increased immunosuppression. Chronic rejection unfolds over months to years, producing intimal thickening of graft vessels, interstitial fibrosis, and progressive organ dysfunction that manifests differently by organ — bronchiolitis obliterans in lung, accelerated atherosclerosis in heart, vanishing bile duct syndrome in liver.
Graft-versus-host disease is the mirror image and appears mainly after bone marrow or other lymphocyte-rich transplants. Here immunocompetent donor T cells attack recipient tissues, classically producing a maculopapular rash, jaundice from liver involvement, and diarrhea. Recognizing that the direction of attack is reversed is the key distinction.
USMLE Step 1 tests rejection heavily in immunology: expect vignettes that give a timeline and biopsy findings and ask you to name the rejection type and its mechanism. The NCLEX approaches the same material from the nursing side, emphasizing recognition of rejection signs, monitoring of immunosuppressive therapy and its infection risk, and care of the transplant patient.
Key takeaways
- Rejection results from recipient immune recognition of donor HLA and ABO antigens.
- Hyperacute rejection occurs within minutes to hours from preformed antibodies and requires graft removal.
- Acute rejection develops over weeks to months, is largely T cell–mediated, and often responds to increased immunosuppression.
- Chronic rejection causes vascular intimal thickening and fibrosis over months to years and is largely irreversible.
- In graft-versus-host disease the donor's T cells attack the recipient, classically causing rash, jaundice, and diarrhea.