Interleukin‐19 ameliorates experimental autoimmune encephalitis

Abstract

Interleukin‐19 serves as a negative feedback regulator to limit the pro‐inflammatory response of macrophages and microglia in autocrine/paracrine manners. Interleukin‐19 suppresses microglia/macrophage antigen presentation, T helper 17 cell expansion and subsequent inflammation in the central nervous system, resulting in improvement in experimental autoimmune encephalomyelitis.