Article
C57BL/6 mice genetically deficient in IL-12/IL-23 and IFN-gamma are susceptible to experimental autoimmune myasthenia gravis, suggesting a pathogenic role of non-Th1 cells.
Journal of immunology (Baltimore, Md. : 1950) - 1 Jun 2007
Wang Wei, Milani Monica, Ostlie Norma, Okita David, Agarwal Rajeev K, Caspi Rachel R, Caspi Rachel, Conti-Fine Bianca M
Abstract excerpt
Immunization with Torpedo acetylcholine receptor (TAChR) induces experimental autoimmune myasthenia gravis (EAMG) in C57BL/6 (B6) mice. EAMG development needs IL-12, which drives differentiation of Th1 cells. The role of IFN-gamma, an important Th1 effector, is not clear and that of IL-17, a proinflammatory cytokine produced by Th17 cells, is unknown. In this study, we examined the effect of simultaneous absence...
Read the complete abstract on PubMedTopics
Share this publication in a Topic to start or enrich a Post.
