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 Blood, 1 April 2008, Vol. 111, No. 7, pp. 3880-3883.
Prepublished online as a Blood First Edition Paper on January 16, 2008; DOI 10.1182/blood-2007-08-107144.

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TRANSFUSION MEDICINE

Brief Report

The TNF (–308A) polymorphism is associated with microchimerism in transfused trauma patients

Ryan M. Gill1,2, Tzong-Hae Lee3, Garth H. Utter4, William F. Reed1,3, Li Wen3, Dan Chafets3, and Michael P. Busch1,3

Departments of1 Laboratory Medicine and 2 Pathology, University of California, San Francisco; 3 Blood Systems Research Institute, San Francisco, CA; and 4 Department of Surgery, University of California, Davis

Microchimerism (MC), defined as the persistence of allogeneic cells at low concentrations, is well documented in transfused trauma patients. We hypothesized that genetic polymorphisms linked to cytokine production could contribute to trauma-induced immune modulation and development of microchimerism after transfusion of trauma patients. We used high-throughput SYBR-green-based genotyping of single nucleotide polymorphisms (SNPs) to characterize 59 transfused trauma patients, with MC (n = 30) and without MC (n = 29), for 4 functionally significant SNPs: TNF (–308), IL 10 (–1082), IFNG (+874), and TGFB1 (+915). We then compared likelihood for development of MC and the magnitude of immune suppression among subjects with and without these selected immune response SNPs. We identified a significant association between TNF (–308A) SNP and both development of MC and diminished immune responsiveness. Hence predisposing genetic factors may explain, in part, why only a subset of trauma patients develops transfusion-associated microchimerism.


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