Professor of Medicine
| Address: | 1825 University Blvd Shelby Building, 305 UAB Birmingham, AL 35294 |
| Telephone: | (205) 934-2472 |
| FAX: | (205) 934-2542 |
| Email: | craman@uab.edu |
| Members of the Laboratory |
| Publications |
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Education
B.Sc. (Zoology), Madras University, India
M.Sc. (Microbiology), Idaho State University
Ph.D. (Microbiology-Immunology), Southern Illinois University
Postdoctoral Studies, Loyola University in Chicago, Stritch School of Medicine, with Dr. Katherine Knight
Research Interests
Dr. Raman’s research 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 context, the research interest of the Raman laboratory is the study of activation and differentiation of effector T cells and B cells in the pathogenesis of these autoimmune disease. Current investigations involve human samples from patients with MS or RA as well mouse models to study these diseases. The major areas of investigation are:
- The mechanisms modulating the activation of T-cells and differentiation to pathogenic (Th1, Th17 and ThIFNγIL-17 –dual producers), regulatory (nTreg, iTreg) Th subsets and cells of the innate immune system (dendritic cells, macrophages and microglia). Within this area of study, the Raman laboratory has a special interest in type 1 and type 2 interferons, and TGFβ family proteins in the pathogenesis of MS, RA and the mouse model, experimental autoimmune encephalomyelitis (EAE)
- Molecular mechanisms by which CK2 and GSK3 modulates effector and regulatory cells in the pathogenesis of autoimmunity
- 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
- TGFβR3/betaglycan dependent regulation of adaptive immune effector cells in the pathogenesis of autoimmune diseases