Differential mediator production by dendritic cells upon toll-like receptor stimulation does not impact T cell cytokine expression.

Dendritic cells are key components of successful immunological responses bridging innate and adaptive defenses. In this study we wanted to know whether ligation of toll-like receptors (TLR) expressed by dendritic cells would induce differential proinflammatory mediator expression and whether these dendritic cells would differentially impact T cell function. For this purpose bone marrow-derived dendritic cells from OTII mice were used. The dendritic cells showed detectable levels of TLR1, 2, 4, 6, 7, 8 and 9, with TLR2 and TLR4 expressed at the highest levels. To determine whether TLR ligation differentially influenced proinflammatory mediator expression the dendritic cells were stimulated with peptidoglycan (PGN) or lipopolysaccharide (LPS) for TLR2 or TLR4, respectively. Comparisons were made to dendritic cells exposed to TNF-alpha or saline as controls. Whereas, both LPS and PGN were equally effective at inducing CXCL1 and TNF-alpha expression from the dendritic cells, LPS was unique at inducing CCL2 expression, and PGN was unique at inducing IL-1beta expression. Despite these differences, LPS and PGN treated dendritic cells were equally effective at eliciting IFN-gamma expression from T cells in an antigen-specific manner. These data indicate that ligation of TLR by components of Gram+ and Gram- bacteria differentially influence dendritic cell proinflammatory mediator expression, and that differential mediator production by dendritic cells upon TLR stimulation does not impact T cell cytokine production.