The McGeachy lab studies mechanisms of activation and regulation of Th17 cells in autoimmune inflammation. In the past decade, Th17 cells have garnered much attention as drivers of tissue inflammation, and therapies to target Th17-associated pathways are making remarkable progress in clinic. Our research is uncovering unexpected roles for both immune and non-immune associated proteins in Th17 biology. For example, in one NIH-funded project we have identified that integrin avß3 is expressed by Th17 cells and is important for their ability to induce inflammation in EAE, the mouse model of multiple sclerosis. Ongoing studies are now investigating the mechanisms through which avß3 integrins regulate Th17 inflammation in different tissues of the body including LN. We are also studying inflammatory T cells in humans with rheumatoid arthritis, in a project recently funded by the Rheumatology Research Foundation to study effects of T cell costimulatory pathway blockade in RA. Biologic therapy in patients offers the opportunity to determine changes in T cells that are related to blockade of specific immune pathways, and we are collaborating with rheumatologists to conduct controlled longitudinal clinical studies to track changes in T cell populations that correspond blockade of TNF, CD28 or IL-6R. The University of Pittsburgh, including the McGeachy lab, is also one of five sites chosen nationally for the NIH/industry/foundation-funded Accelerating Medicines Partnership, which aims to dissect the immune networks that are active in different cellular populations isolated from RA joint tissues using state-of-the-art assays and bioinformatics.