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Host immune responses to donor antigens constitute one of many major mechanisms underlying chronic rejection of transplanted organs [1]. Matching MHC antigens reduces anti-donor T-cell responses and improves long-term survival of allografts, like kidneys [2], but will not supply total tolerance nor obviate the will need for lifelong immunosuppressive therapy [3,4], which in itself can contribute to transplant dysfunction and demise [5].PMID:24406011 Diverse non-MHC polymorphisms across the donor genome give rise to minor histocompatibility (H) antigens, which, excepting these encoded by mitochondrial DNA, are presented by classical class I and II molecules to alloreactive T cells [6]. When the frequency of T cells recognizing these epitopes is only a tiny fraction of these that react to donor MHC molecules, most minor H antigen disparities in outbred populations can’t readily be circumvented by matching, and consequently, these donor-reactive T-cell responses might be clinically significant causes of rejection [7]. A variety of immunomodulatory agents, generally in mixture, are.
