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Roles of Toll-Like Receptors in Allogeneic Islet Transplantation

Authors
 Han Ro ; Juho Hong ; Jaeseok Yang ; Curie Ahn ; Kook-Hwan Oh ; Jong Cheol Jeong ; Eun Mi Lee ; Hye-Jung Yeom ; Kyu Hyun Han ; Myung-Gyu Kim ; Eun Won Lee ; Beom Seok Kim 
Citation
 Transplantation, Vol.94(10) : 1005~1012, 2012 
Journal Title
 Transplantation 
ISSN
 0041-1337 
Issue Date
2012
Abstract
Background: Toll-like receptors (TLRs) are involved in the rejection of solid organ allografts. However, the roles of TLRs in islets are still controversial. We investigated the roles of TLRs in donor islets together with those in recipients in allogeneic islet transplantation. Methods: To assess the roles of TLRs in either donor islets or recipients, allogeneic islet transplantation was performed using myeloid differentiation factor 88 (MyD88)-knockout (KO), TLR4-KO, or Toll/interleukin-1 receptor domain-containing adaptor-inducing interferon-[beta] (TRIF)-KO mice. Results: Both polyriboinosinic polyribocytidylic acid and lipopolysaccharide (LPS) stimulation induced the mRNA expression of regulated and normal T cell expressed and secreted, interferon-[gamma]–inducible protein-10, monocyte chemotactic protein-1, interleukin-8, and inducible nitric oxide synthase in murine islets, whereas the induction was attenuated in TRIF-KO, interferon-[beta] promoter stimulator-1-KO, and TLR4-KO mice. When islets from MyD88-KO, TLR4-KO, or TRIF-KO C57BL/6 mice were transplanted to BALB/c recipients, graft survival was not better than that of wild-type (WT) islets. However, the survival of the MyD88-KO islet allograft was significantly prolonged when combined with anti-CD40L. In parallel, LPS stimulation in donor islets interfered with anti-CD40L blockade-mediated long-term survival of islet allografts in TLR4-KO recipients. LPS stimulation increased the perigraft infiltration of both T cells and macrophages. Then again, when islets from WT BALB/c mice were transplanted to MyD88-KO, TRIF-KO, or WT C57BL/6 mice, there was no difference in graft survival, although some of the MyD88-KO recipients obtained long-term graft survival. However, anti-CD40L prolonged graft survival significantly in MyD88-KO recipients. The absence of MyD88 in either donors or recipients decreased the perigraft infiltration of inflammatory cells when combined with anti-CD40L. Conclusions: TLRs in both donor islets and recipients are involved in islet allograft rejection.
URI
http://ir.ymlib.yonsei.ac.kr/handle/22282913/91949
DOI
10.1097/TP.0b013e3182708dd3
Appears in Collections:
1. 연구논문 > 1. College of Medicine > Dept. of Internal Medicine
Yonsei Authors
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 http://ovidsp.ovid.com/ovidweb.cgi?T=JS&CSC=Y&NEWS=N&PAGE=fulltext&AN=00007890-201211270-00005&LSLINK=80&D=ovft
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