Background:
Toll-like receptor 5 (tlr5) is implicated in the innate and adaptive immune responses that are associated with inflammatory bowel disease (ibd). in humans tlr5 is expressed on cd4(+) t cells and costimulation with flagellin potentiates effector and regulatory t cell responses. the aim of this study was to determine the role of tlr5 in cd4(+) t cell subsets versus other cells in induction of disease in a model of t cell-dependent colitis.
Methods:
Tlr5 expression on cd4(+) t cells was assessed by real-time reverse-transcriptase polymerase chain reaction (rt-pcr). wildtype (wt) or tlr5-deficient (5-/-) cd4(+) t conventional cells (tconv) and t regulatory cells (treg) were compared for their ability to induce and suppress t cell transfer colitis, respectively. in addition, the role of tlr5 expression in recipient mice was analyzed.
Results:
Tlr5 is preferentially expressed on mouse treg compared to tconv, although expression levels were low. the colitogenic capacity of wt and 5-/- tconv was found to be similar and treg from wt or 5-/- donor animals both prevented t cell transfer colitis in tlr-competent hosts. tlr5 deficiency in recipient mice, however, did affect the disease process, as t cell receptor-β (tcrβ) 5-/- recipients had decreased weight loss compared to tcrβ recipient mice when wt tconv were used.
Conclusions:
Tlr5 expression on t cells is not required for induction of or protection from t cell-dependent colitis. expression of tlr5 in non-t cells has a pathogenic role, since tlr5 deficiency in recipient mice protects against weight loss induced by wt t cells.