2002年10月
Toll-like receptor 2 contributes to liver injury by Salmonella infection through Fas ligand expression on NKT cells in mice
Gastroenterology
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- 巻
- 123
- 号
- 4
- 開始ページ
- 1265
- 終了ページ
- 1277
- 記述言語
- 英語
- 掲載種別
- 研究論文(学術雑誌)
- DOI
- 10.1053/gast.2002.36006
- 出版者・発行元
- W B SAUNDERS CO
Background & Aims: Toll-like receptors (TLRs) for bacterial constitutes are expressed not only by phagocytes but also by some subsets of T cells. We previously reported that natural killer T cells (NKT cells) play an important role in liver injury induced by Salmonella infection. In the present study, we investigated whether TLRs on NKT cells are involved in Salmonella-induced liver injury. Methods: Gene expression of TLR2 was examined in sorted natural killer, NKT, and T cells from livers of naive mice by the reverse-transcription polymerase chain reaction method. Serum alanine aminotransferase level and FasL expression on liver lymphocytes were examined in TLR2-deficient (TLR2-/-) and FasL-deficient gld/gld mice before and after intraperitoneal inoculation of Salmonella choleraesuis 31N-1 using an enzyme-linked immunosorbent assay and flow cytometry. Results: TLR2 gene was abundantly expressed by NKT cells freshly isolated from naive mice. FasL expression on liver NKT cells increased in TLR2+/- mice but not in TLR2-/- mice after Salmonella infection. Serum alanine aminotransferase level was significantly lower in the TLR2-/- and gld/gld mice than in the control mice after infection. Conclusions: TLR2 may contribute to liver injury induced by Salmonella infection via FasL induction on liver NKT cells.
- リンク情報
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- DOI
- https://doi.org/10.1053/gast.2002.36006
- PubMed
- https://www.ncbi.nlm.nih.gov/pubmed/12360487
- Web of Science
- https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000178415800037&DestApp=WOS_CPL
- Scopus
- https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=0036789130&origin=inward
- Scopus Citedby
- https://www.scopus.com/inward/citedby.uri?partnerID=HzOxMe3b&scp=0036789130&origin=inward
- ID情報
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- DOI : 10.1053/gast.2002.36006
- ISSN : 0016-5085
- PubMed ID : 12360487
- SCOPUS ID : 0036789130
- Web of Science ID : WOS:000178415800037