Rheumatologic disorders such as arthritis (e.g. rheumatoid arthritis) and/or uveitis (a frequent extra-articular manifestation in rheumatic syndromes) affect millions of individuals in the United States who suffer from pain and disability. Research efforts in the Rosenzweig Lab support a new paradigm that autoimmunity develops from complex environmental and genetic interactions. The lab's research efforts have shown that innate immune receptors such as NOD-like receptors (NLRs) or the C-type lectin receptors (CLRs), which are typically involved in host defense against bacterial and fungal infection, participate in localized tissue injury responses within the eye and joint.
The lab has recently extended this work to uncover how NLRs and CLRs can also potentiate development of autoreactive T cells, Th17 differentiation and autoimmune disease. Current projects seek to delve into the mechanisms by which NLRs or CLRs might regulate pathogenic "rogue" T cell responses and serve in protection against development of autoreactive T cells and potentiate T cell-mediated disease.
The lab's cross-disciplinary approach encompasses functional genetics, mechanisms that regulate autoreactive T cells, cellular and immunological approaches to study clinically relevant diseases such as arthritis and uveitis. Cutting edge technology is employed to further study clinically-relevant disease readouts, including near-infrared (NIR) imaging of molecular events within arthritic joints, live Intravital videomicroscopy imaging of on-going cell trafficking responses within the eye in vivo, and topical endoscopy fundus imaging of the neuroretina.