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Graft-versus-host disease (GVHD) is a common complication that is caused by donor T cells following allogeneic hematopoietic cell transplant. Recently, the functional state of T cells has been characterized by their chemokine receptor expression pattern [1]. T cells expressing chemokine receptor CCR5 contribute to the rejection of solid organ allografts [2] and development of murine GVHD [3-5]. A nonfunctional mutant allele of CCR5, CCR5Δ32, is found with 10% frequency in Caucasians [6,7]. In a study of renal-transplant survival, patients homozygous for CCR5Δ32 had significantly prolonged graft survival compared to heterozygous or wild-type patients [8].
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Ma et al. (2009) studied this question.
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