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Abstract Because aGVHD occurs in approximately 30% of HLAidentical sibling transplants, molecules other than major histocompatibility complex (MHC), generally referred to as minor histocompatibility antigens, could be responsible for the developement of aGVHD. CD31 is a candidate human mHag relevant to acute GVHD, but reports disagree about its level of significance. Therefore, we examined the impact of CD31matching on the outcome of HSCT in different hematological and immunological diseases. donorpatient CD31 codon 125 nonidentity is a significant risk factor for severe acute GVHD and relapse in HLAidentical sibling bone marrow transplant. Typing of these loci by simple molecular biology techniques could ameliorate the outcome of allogeneic BMT. When more than one HLAmatched donor is available, testing of mHa could be used to select the most closely related to the recipient, whereas when a single donor is available the degree of genetic disparity could be used to adjust aGVHD prophylaxis. |