Abstract
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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 3880-3883 |
| Number of pages | 4 |
| Journal | Blood |
| Volume | 111 |
| Issue number | 7 |
| DOIs | |
| State | Published - Apr 1 2008 |
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ASJC Scopus subject areas
- Hematology
- Biochemistry
- Cell Biology
- Immunology
Cite this
The TNF (-308A) polymorphism is associated with microchimerism in transfused trauma patients. / Gill, Ryan M.; Lee, Tzong Hae; Utter, Garth H; Reed, William F.; Wen, Li; Chafets, Dan; Busch, Michael P.
In: Blood, Vol. 111, No. 7, 01.04.2008, p. 3880-3883.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - The TNF (-308A) polymorphism is associated with microchimerism in transfused trauma patients
AU - Gill, Ryan M.
AU - Lee, Tzong Hae
AU - Utter, Garth H
AU - Reed, William F.
AU - Wen, Li
AU - Chafets, Dan
AU - Busch, Michael P.
PY - 2008/4/1
Y1 - 2008/4/1
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=43549118444&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=43549118444&partnerID=8YFLogxK
U2 - 10.1182/blood-2007-08-107144
DO - 10.1182/blood-2007-08-107144
M3 - Article
C2 - 18199828
AN - SCOPUS:43549118444
VL - 111
SP - 3880
EP - 3883
JO - Blood
JF - Blood
SN - 0006-4971
IS - 7
ER -