Pathology Cheat Sheet
Recognising Self, Graft, and Target
HLA, transplant rejection and autoimmunity for NEET-PG: MHC class I vs II, hyperacute vs acute vs chronic rejection, GVHD, tolerance, and molecular mimicry.
MedNext Academy | 3 min read
Recognising Self, Graft, and Target
HLA, transplant rejection and autoimmunity for NEET-PG: MHC class I vs II, hyperacute vs acute vs chronic rejection, GVHD, tolerance, and molecular mimicry.
The HLA system, transplant rejection mechanisms, and the breakdown of tolerance that causes autoimmunity.
High-yield lines
- The HLA system is the human major histocompatibility complex located on chromosome 6.
- HLA class I comprises A, B, and C and presents to CD8 cells, while class II comprises DR, DP, and DQ and presents to CD4 cells.
- An allograft between different individuals of the same species is subject to rejection unless immunosuppressed.
- Hyperacute rejection occurs within minutes due to preformed donor-specific antibodies causing complement-mediated endothelial thrombosis.
- Acute rejection is cell-mediated and antibody-mediated and typically responds to increased immunosuppression.
- Chronic rejection produces progressive vascular intimal thickening and graft fibrosis via indirect allorecognition.
- ABO compatibility and crossmatch testing prevent hyperacute rejection in solid organ transplantation.
- Graft-versus-host disease occurs when donor T cells attack an immunosuppressed recipient, affecting skin, gut, and liver.
- Autoimmunity results from failure of self-tolerance through defects in central or peripheral tolerance.
- Molecular mimicry, where microbial antigens resemble self-antigens, is a mechanism of autoimmunity.
- HLA-DR4 is associated with rheumatoid arthritis and HLA-B27 with ankylosing spondylitis.
- Central tolerance deletes autoreactive lymphocytes in the thymus and bone marrow, while peripheral tolerance uses anergy and regulatory T cells.
Mapped competency codes
- PA9.3
- PA9.4
- PA9.7
Continue into the full chapter
This summary maps to PA9-immunopathology-and-aids.
Frequently Asked Questions
What causes hyperacute graft rejection?
Preformed donor-specific antibodies against donor HLA or ABO antigens that bind endothelium within minutes, activating complement and causing thrombosis and ischaemic graft necrosis.
What is the difference between HLA class I and class II?
Class I (A, B, C) is on all nucleated cells and presents endogenous peptides to CD8 T cells, while class II (DR, DP, DQ) is on antigen-presenting cells and presents exogenous peptides to CD4 T cells.
What is molecular mimicry in autoimmunity?
A mechanism in which a microbial antigen closely resembles a self-antigen, so the immune response against the microbe cross-reacts with host tissue.
What is graft-versus-host disease?
A condition in which immunocompetent donor T cells attack the tissues of an immunosuppressed recipient, classically damaging the skin, gastrointestinal tract, and liver.
Continue reading
Cheat SheetsAll Pathology cheat sheets
Browse the complete authored set for this subject.
Open the complete revision pathway
Explore clinician-written learning resources, structured revision and practice across the MedNext platform.
Open in the MedNext appSee plans

