Limiting the severity of inflammation and its eventual resolution are critical pathways which are vital to minimizing damage to host tissues. We study the ability of the biologics otelixizumab (anti-CD3) and adalimumab (anti-TNF) to induce a potent CD8+FOXP3+ regulatory T cell (Treg) population in rheumatoid arthritis patients. These Treg can suppress CD4+ T cell proliferation and IL-17 and IFN-γ production; however their mechanism of action is unknown. We have been studying how monocytes are crucial for the induction of FOXP3 expression in CD8+ T cells and how CD8+ T cells can control their ability to become a Treg via p38 phosphorylation.

Our studies aim to 1) identify novel therapeutic targets that may mimic Treg function or 2) enhance the efficacy of biologic drugs used in the clinic to treat RA and type 1 diabetes by the use of combination therapy.