TLR2, TLR3, TLR4, TLR9 and TLR11 expression on effector CD4+T-cell subsets in Leishmania donovani infection

T-cells play a central role in cell-mediated immunity. While activation of T-cells is major histocompatibilityrestricted, the Toll-like receptors (TLRs)-a family of proteins that recognize conserved molecular patterns present on the pathogens-are not well-studied for their expression and function in T-cells. As any association of TLR expression profiles with an effector T-cell subset is unknown, we analyze BALB/c mice-derived CD4+ and CD8+ T-cells' TLR expression profiles. We report: CD4+t-bet+ T-cells are frequent in TLR2LowTLR3HighTLR4Low sub population, CD4+GATA3+ T-cells are frequent within the cells with intermediate expression of TLR2, TLR3, TLR4 and TLR11, CD4+FoxP3+ T-cells in TLR2HighTLR3High cells whereas CD4+ROR gamma t +T-cells are frequent in TLR2LowTLR3LowTLR4LowTLR11Low cells. CD4+ effector T-cell subsets may therefore show association with TLRsTLR3, in particular-expression. In Leishmania donovani infection in BALB/c mice, TLR3 expression on both CD4+ and CD8+ T-cells is reduced. Poly-I:C, a TLR3 ligand, do not have any distinctive effects on the CD4+ effector T cell subsets. These data suggest that TLRs on T-cells may not function as a primary receptor that controls T-cell function but their distinctive expression profiles on different T-cell subsets suggest plausible immunomodulatory role.