How do T h17 cells mediate autoimmune inflammation in the central nervous system?

Th17 cells were first discovered in the context of autoimmunity, but it is likely that this subset of T  helper cells has its primary function in host defense of pathogens, such as particular fungi against which T h1 or T h2 responses are not protective. In the early days of T h17 research, a great deal of effort was made to prove the identity of T h17 cells as a distinct lineage of T helper cells independent of T h1 and T h2 cells. However, T h17 cells are increasingly considered as a plastic subset of T  helper cells that can co‐produce interleukin‐17 with interferon‐γ or interleukin‐17 with interleukin‐10 and then usurp T ‐bet or c‐Maf as transcription factors that have been regarded as private to T h1 or T h2 cells, respectively. A coherent concept to explain the importance of T h17 cells in a series of autoimmune diseases including psoriasis, rheumatoid arthritis and multiple sclerosis is still missing. However, the prominent role of T h17 cell responses at epithelial surfaces (like the gut) where the discrimination between self and foreign is particularly challenging might contribute to the predominant T h17 skewing of autoreactive T  cells when immune tolerance is broken. In the present review, some novel aspects on the generation and biological properties of T h17 cells including trafficking and effector functions with particular emphasis on autoimmunity in the central nervous system are highlighted.