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 histocompatibility-restricted, 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 TLR2^LowTLR3^HighTLR4^Low subpopulation, CD4⁺GATA3⁺ T-cells are frequent within the cells with intermediate expression of TLR2, TLR3, TLR4 and TLR11, CD4⁺FoxP3⁺ T-cells in TLR2^HighTLR3^High cells whereas CD4⁺RORγt ⁺ T-cells are frequent in TLR2^LowTLR3^LowTLR4^LowTLR11^Low cells. CD4⁺ effector T-cell subsets may therefore show association with TLRs- TLR3, 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.