IL-23 and Th17 cells in infections and psoriasis

Abstract

IL-3 is produced by dendritic cells, and other antigen presenting cells. IL-23 is required for the induction, expansion, maintenance and downstream effector functions of Th17 cells. Th17 cells upregulate neutrophil chemokines, antimicrobial peptides, and other pro-inflammatory cytokines. The lack of Th17 cells results in susceptibility to Candida, Streptococcal and Staphylococcal infections. On the contrary, the excess of Th17 cells induce various autoimmune diseases such as psoriasis. Several studies revealed that infections were more common in psoriatics than in healthy individuals. Superantigens released by microorganisms have been suggested as exogenous triggers that stimulate T cells to initiate psoriasis. Understanding the Th17 responses and their interactions with the immune system will likely provide crucial insights in the host defense and autoimmune diseases like psoriasis, and this will provide new tools for the development of e.ective immunomodulatory treatment strategies for infectious diseases and autoimmune diseases. © 2011 The Japan Society for Clinical Immunology.