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TLR5-Deficient Mice Lack Basal Inflammatory and Metabolic Defects but Exhibit Impaired CD4 T Cell Responses to a Flagellated Pathogen
Author(s) -
Shirdi Letran,
Seung–Joo Lee,
Shaikh M. Atif,
Adriana FloresLangarica,
Satoshi Uematsu,
Shizuo Akira,
Adam F. Cunningham,
Stephen J. McSorley
Publication year - 2011
Publication title -
the journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.737
H-Index - 372
eISSN - 1550-6606
pISSN - 0022-1767
DOI - 10.4049/jimmunol.1003576
Subject(s) - tlr5 , flagellin , biology , inflammation , basal (medicine) , pathogen , immunology , phenotype , microbiology and biotechnology , endocrinology , gene , genetics , tlr4 , tlr2 , insulin
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.

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