Interleukin-17A (IL-17A) is produced by T helper cells, binds to the receptor IL-17RA and acts synergistically with TNFa and interleukin-1. The most notable role of IL-17A is its involvement in inducing and mediating proinflammatory responses. IL-17A induces the production of many cytokines, chemokines, prostaglandins from many cell types (e.g. fibroblasts, macrophages). Therefore the IL-17 family has been linked to autoimmune related diseases including rheumatoid arthritis. Here we investigated whether the inflammatory mediator IL-17A influences dorsal root ganglia (DRG) neurons. In DRGs the expression of the IL-17RA was analyzed using a specific anti-IL17RA antibody and also by PCR. To describe the influence of IL-17A in DRG neurons we added IL-17A (1 nmol/l) to cultured neurons for two days. Thereafter the cells were fixed and analyzed for the expression of pERK, NFkB, COX-1, COX-2 and TRPV4 using specific antibodies. In addition capsaicin-induced cobalt-uptake with and without preincubation with IL-17 was done. In DRG sections 86.2 ± 6.3 % of all neurons showed IL-17RA-like IR and also peripheral processes and many satellite cells were labeled. We found PCR products of IL-17RA in total DRGs and also in cultured DRG neurons. In addition we found IL-17A RT-PCR products in DRGs 8 h after induction of an arthritis. The expression of COX-1, COX-2 and the capsaicin-induced cobalt-uptake was not altered by IL-17A. But we found a significant up-regulation of pERK-, NFkB- and TRPV4-like IR in neurons preincubated with IL-17A. We conclude therefore that DRG neurons may be a significant target for IL-17A actions.