Dr. Raman’s laboratory interrogates molecular and cellular mechanisms driving the immunopathogenesis of autoimmune diseases with a special emphasis on multiple sclerosis (MS) and rheumatoid arthritis (RA). Within this are of research, the current studies focus on molecular mechanisms underlying activation and differentiation of effector T cells, B cells and innate cells in the pathogenesis of these autoimmune diseases. Current investigations involve human immunology bridged with mouse models to study RA and MS. The major area of investigation is immunopathogenesis of multiple sclerosis. We have several interrelated projects in this area of investigation:
i. Type 1 IFNs (IFN-α and IFN-β) and type 2 IFN (IFN-γ) in pathogenesis and regulation of MS and RA – Our studies primarily focuses on outcomes of signaling from the IFN receptors in different innate and adaptive immune cell populations. Our immunopathogenic mechanism driving progression of multiple sclerosis (MS) that involves human studies and the mouse model, experimental autoimmune encephalomyelitis (EAE).
ii. Molecular mechanisms by which CK2 and GSK3 modulates effector and regulatory cells in the pathogenesis of autoimmunity.
iii. Role of CD5 in T cell and B-1a B cell development, differentiation, immunity and pathogenesis – the laboratory focuses on B-1a B cell-dependent T-independent antibody responses, T-dependent antibody responses, autoreactive B-cell generation and persistence and regulatory B-cells. For these studies, the Raman laboratory has generated unique knock-in CD5 mutant mice in which signaling domains associated with CD5-inhibitory activity (ITIM) and CD5-CK2 activation have been ablated.
iv. TGFβR3/betaglycan dependent regulation of adaptive immune effector cells in the pathogenesis of autoimmune diseases