## Acute Cellular Rejection Pathophysiology **Key Point:** Acute cellular rejection (ACR) is the most common form of acute rejection and is mediated by T cell responses, particularly CD8+ cytotoxic T lymphocytes (CTLs). ### Mechanism 1. Donor MHC class I antigens are recognized directly by recipient CD8+ T cells 2. CD4+ helper T cells also contribute by recognizing donor MHC class II antigens 3. Activated T cells infiltrate the graft and cause tissue destruction 4. Occurs days to months post-transplantation ### Histopathology - Interstitial and perivascular lymphocytic infiltration - Endothelialitis (lymphocyte infiltration of vessel walls) - Tubulitis (in renal allografts) - Tissue necrosis and edema **High-Yield:** ACR is the most common cause of acute graft dysfunction and is potentially reversible with immunosuppressive therapy (unlike hyperacute rejection). ### Comparison with Other Rejection Types | Rejection Type | Timing | Primary Mediator | Reversibility | |---|---|---|---| | Hyperacute | Minutes to hours | Pre-formed IgG antibodies (complement-dependent) | No | | Acute Cellular | Days to months | CD8+ CTLs, CD4+ T cells | Yes | | Acute Antibody | Days to months | Donor-specific antibodies (DSA) | Partial | | Chronic | Months to years | T cells + antibodies + immune-independent factors | No | **Clinical Pearl:** Acute cellular rejection can be diagnosed by graft biopsy showing lymphocytic infiltration and treated with pulse corticosteroids or anti-T cell antibodies (OKT3, ATG).
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