Abstract
Interleukin (IL)-17-producing helper T cells may play a pivotal role in the pathogenesis of multiple sclerosis. Here, we examined the effects of IL-17 on microglia, which are known to be critically involved in multiple sclerosis. Treatment with IL-17 upregulated the microglial production of IL-6, macrophage inflammatory protein-2, nitric oxide, adhesion molecules, and neurotrophic factors. We also found that IL-17 was produced by microglia in response to IL-23 or IL-1beta. Because microglia produce IL-1beta and IL-23, these cytokines may act in an autocrine manner to induce IL-17 expression in microglia, and thereby contribute to autoimmune diseases, such as MS, in the central nervous system.