TLR5-deficient mice lack basal inflammatory and metabolic defects but exhibit impaired CD4 T cell responses to a flagellated pathogen
SE Letran, SJ Lee, SM Atif… - The Journal of …, 2011 - journals.aai.org
The Journal of Immunology, 2011•journals.aai.org
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 …
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 …
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.
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