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Roles of Toll-Like Receptors in Allogeneic Islet Transplantation

DC FieldValueLanguage
dc.contributor.author김범석-
dc.date.accessioned2014-12-19T17:43:54Z-
dc.date.available2014-12-19T17:43:54Z-
dc.date.issued2012-
dc.identifier.issn0041-1337-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/91949-
dc.description.abstractBackground: 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.-
dc.description.statementOfResponsibilityopen-
dc.relation.isPartOfTRANSPLANTATION-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAdaptor Proteins, Vesicular Transport/deficiency-
dc.subject.MESHAdaptor Proteins, Vesicular Transport/genetics-
dc.subject.MESHAdaptor Proteins, Vesicular Transport/physiology*-
dc.subject.MESHAnimals-
dc.subject.MESHChemokine CCL2/metabolism-
dc.subject.MESHChemokine CXCL10-
dc.subject.MESHGraft Rejection/physiopathology*-
dc.subject.MESHGraft Survival/physiology-
dc.subject.MESHIn Vitro Techniques-
dc.subject.MESHInterleukin-8/metabolism-
dc.subject.MESHIslets of Langerhans/drug effects-
dc.subject.MESHIslets of Langerhans/metabolism-
dc.subject.MESHIslets of Langerhans Transplantation/physiology*-
dc.subject.MESHLipopolysaccharides/pharmacology-
dc.subject.MESHMice-
dc.subject.MESHMice, Inbred BALB C-
dc.subject.MESHMice, Inbred C57BL-
dc.subject.MESHMice, Knockout-
dc.subject.MESHModels, Animal-
dc.subject.MESHMyeloid Differentiation Factor 88/deficiency-
dc.subject.MESHMyeloid Differentiation Factor 88/genetics-
dc.subject.MESHMyeloid Differentiation Factor 88/physiology*-
dc.subject.MESHNitric Oxide Synthase Type II/metabolism-
dc.subject.MESHTissue Donors*-
dc.subject.MESHToll-Like Receptor 4/deficiency-
dc.subject.MESHToll-Like Receptor 4/genetics-
dc.subject.MESHToll-Like Receptor 4/physiology*-
dc.subject.MESHTransplantation*-
dc.subject.MESHTransplantation, Homologous/physiology-
dc.titleRoles of Toll-Like Receptors in Allogeneic Islet Transplantation-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Internal Medicine (내과학)-
dc.contributor.googleauthorHan Ro-
dc.contributor.googleauthorJuho Hong-
dc.contributor.googleauthorBeom Seok Kim-
dc.contributor.googleauthorEun Won Lee-
dc.contributor.googleauthorMyung-Gyu Kim-
dc.contributor.googleauthorKyu Hyun Han-
dc.contributor.googleauthorHye-Jung Yeom-
dc.contributor.googleauthorEun Mi Lee-
dc.contributor.googleauthorJong Cheol Jeong-
dc.contributor.googleauthorKook-Hwan Oh-
dc.contributor.googleauthorCurie Ahn-
dc.contributor.googleauthorJaeseok Yang-
dc.identifier.doi23169223-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA00488-
dc.relation.journalcodeJ02754-
dc.identifier.eissn1534-6080-
dc.identifier.pmid23169223-
dc.identifier.urlhttp://ovidsp.ovid.com/ovidweb.cgi?T=JS&CSC=Y&NEWS=N&PAGE=fulltext&AN=00007890-201211270-00005&LSLINK=80&D=ovft-
dc.subject.keywordDonor-
dc.subject.keywordIslet transplantation-
dc.subject.keywordRecipient-
dc.subject.keywordRejection-
dc.subject.keywordToll-like receptor-
dc.contributor.alternativeNameKim, Beom Seok-
dc.contributor.affiliatedAuthorKim, Beom Seok-
dc.citation.volume94-
dc.citation.number10-
dc.citation.startPage1005-
dc.citation.endPage1012-
dc.identifier.bibliographicCitationTRANSPLANTATION, Vol.94(10) : 1005-1012, 2012-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers

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