TLR5-deficient mice lack basal inflammatory and metabolic defects but exhibit impaired CD4 T cell responses to a flagellated pathogen

Shirdi E. Letran, Seung Joo Lee, Shaikh M. Atif, Adriana Flores-Langarica, Satoshi Uematsu, Shizuo Akira, Adam F. Cunningham, Stephen J Mcsorley

Research output: Contribution to journalArticle

53 Scopus citations

Abstract

TLR5-deficient mice have been reported to develop spontaneous intestinal inflammation and metabolic abnormalities. However, we report that TLR5-deficient mice from two different animal colonies display no evidence of basal inflammatory disease, metabolic abnormalities, or enhanced resistance to Salmonella infection. In contrast, the absence of TLR5 hindered the initial activation and clonal expansion of intestinal flagellin-specific CD4 T cells following oral Salmonella infection. Together, these data demonstrate that a basal inflammatory phenotype is not a consistent feature of TLR5-deficient mice and document a novel role for TLR5 in the rapid targeting of flagellin by intestinal pathogen-specific CD4 T cells.

Original languageEnglish (US)
Pages (from-to)5406-5412
Number of pages7
JournalJournal of Immunology
Volume186
Issue number9
DOIs
StatePublished - May 1 2011
Externally publishedYes

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ASJC Scopus subject areas

  • Immunology

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