IK acts as an immunoregulator of inflammatory arthritis by suppressing T_H17 cell differentiation and macrophage activation.

ABSTRACT: Pathogenic T helper cells (T_H) and macrophages have been implicated in the development of rheumatoid arthritis (RA), which can lead to severe synovial inflammation and bone destruction. A range of therapies have been widely used for RA, including specific monoclonal antibodies and chemical inhibitors against inflammatory cytokines produced by these cells. However, these have not been sufficient to meet the medical need. Here, we show that in transgenic mice expressing truncated IK (tIK) cytokine, inflammatory arthritis symptoms were ameliorated as the result of suppression of the differentiation of T_H1 and T_H17 cells and of macrophage activation. During inflammatory responses, tIK cytokine systemically regulated macrophage functions and T_H17 cell

SUBMITTER: Park HL 

PROVIDER: S-EPMC5223115 | biostudies-literature | 2017 Jan

REPOSITORIES: biostudies-literature