| Literature DB >> 26413419 |
Nicole L Glosson-Byers1, Sarita Sehra2, Mark H Kaplan1.
Abstract
STAT4 is a critical mediator of inflammatory immunity and is required for all known IL-12 biological responses, including the induction of IFN-γ and development of Th1 cells. We demonstrate that IL-23, an IL-12-related cytokine, also requires STAT4 for optimal IL-17 secretion from memory T helper cells and NKT cells. Although IL-23 stimulation had modest effects on STAT4 activation, STAT4-deficiency results in reduced Il23r expression. These data demonstrate a restricted requirement for STAT4 in innate and adaptive IL-17-secreting T cell responses that might contribute to inflammatory immunity.Entities:
Keywords: IL-23R; NKT; STAT4; Th17; memory Th
Year: 2014 PMID: 26413419 PMCID: PMC4580079 DOI: 10.4161/21623988.2014.955393
Source DB: PubMed Journal: JAKSTAT ISSN: 2162-3988