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Kamal D Moudgil
M.D., Ph.D.
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| Academic Title:
Associate Professor |
| Primary Appointment:
Microbiology and Immunology |
| Secondary Appointments:
Medicine |
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kmoud001@umaryland.edu |
| Location:
HH
323C |
| Phone:
(410) 706-7804 (office) |
| Phone:
(410) 706-7918 (lab) |
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Research Interests
My research interests are focused on two areas: 1) antigen processing and presentation, and 2) the induction and regulation of autoimmune arthritis. Using mouse lysozyme (ML) as a model self antigen, we have shown that mice are tolerant to native ML but possess T cells potentially directed against hidden (cryptic) determinants within ML. We are presently examining the influence of the hierarchy (dominance/crypticity) of self determinants on shaping of the T cell repertoire in the thymus, and the role of the anti-cryptic T cell repertoire in the induction of autoimmunity. These studies are being conducted in mice lacking ML-M. Also under investigation is the role of CD4+CD25+ regulatory T cells in tolerance to ML-M. In parallel, studies are underway in the rat adjuvant arthritis (AA) model of human rheumatoid arthritis. We have shown that during the course of AA in the Lewis rat, there is diversification of the T cell response to carboxy-terminal determinants within the 65-kD heat-shock protein (hsp65). Interestingly, unlike in models of other autoimmune diseases, this diversification of response is regulatory rather than being pathogenic. The mechanism of diversification of response to hsp65 and its involvement in natural remission from acute AA in Lewis rats; the immunologic basis of susceptibility/resistance to AA of rat strain(s) that have the same class II MHC haplotype; and characterization of the antigen reactivity of synovial-infiltrating T cells are the focus of my current research in AA. A novel aspect spanning these studies relates to the role of self hsp65 in regulation of AA. The results of these studies would contribute significantly to understanding of the pathogenesis of autoimmune diseases, and to devising novel therapeutic strategies for these disorders.
Publications
Jiang, X. and K. D. Moudgil. 2006. The unveiling of hidden T cell determinants of a native antigen by defined mediators of inflammation: implications for the pathogenesis of autoimmunity. Scand. J. Immunol. 63: 338.
Zhu, H., K. Liu, J. Cerny, T. Imoto, and K. D. Moudgil. 2005. Insertion of the dibasic motif in the flanking region of a cryptic self-determinant leads to activation of the epitope-specific T cells. J Immunol 175:2252.
Mia, M. Y., M. Durai, H. R. Kim, and K. D. Moudgil. 2005. Heat shock protein 65-reactive T cells are involved in the pathogenesis of non-antigenic dimethyl dioctadecyl ammonium bromide-induced arthritis. J Immunol 175:219.
Moudgil, K. D., and E. E. Sercarz. 2005. Understanding crypticity is the key to revealing the pathogenesis of autoimmunity. Trends Immunol 26:355.
Fan, A. Y., L. Lao, R. X. Zhang, A. N. Zhou, L. B. Wang, K. D. Moudgil, D. Y. Lee, Z. Z. Ma, W. Y. Zhang, and B. M. Berman. Effects of an acetone extract of Boswellia carterii Birdw. (Burseraceae) gum resin on adjuvant-induced arthritis in Lewis rats. J. Ethnopharmacol. 2005, 101: 104.
Durai, M., H.R. Kim, and K.D. Moudgil. The regulatory C-terminal determinants within mycobacterial heat shock protein 65 are cryptic and cross-reactive with the dominant self homologs: implications for the pathogenesis of autoimmune arthritis. J. Immunol. 2004, 173: 181.
Sinha, P., H.H. Chi, H.R. Kim, B.E. Clausen, B. Pederson, E.E. Sercarz, I. Forster and K.D. Moudgil. Mouse lysozyme-M knockout mice reveal how the self determinant hierarchy shapes the T cell repertoire against this circulating self antigen in wild type mice. J. Immunol. 2004, 173: 1763.
Durai, M., R.S. Gupta, and K.D. Moudgil. The T cells specific for the carboxyl-terminal determinants of self(rat) heat-shock protein 65 escape tolerance induction and are involved in regulation of autoimmune arthritis. J. Immunol. 2004, 172: 2795.
Moudgil, K.D. and M. Durai. Epitope Spreading. Infection and Autoimmunity (eds. Y. Shoenfeld and N. R. Rose), Elsevier, Amsterdam, The Netherlands, 2004, p.19-43.
Stevens D.B., D.P. Gold, E.E. Sercarz, and K.D. Moudgil. The Wistar Kyoto rat (RT.1l) is resistant to myelin basic protein-induced experimental autoimmune encephalomyelitis: comparison with the susceptible Lewis (RT1l) strain with regard to the MBP-directed CD4+ T cell repertoire and its regulation. J. Neuroimmunol. 2002, 126: 25.
Melo ME, Gabaglia CR, Moudgil KD, Sercarz EE, Quinn A. Strain-dependent effect of nasal instillation of antigen on the immune response in mice. Isr Med Assoc J 2002; 4: 902.
Moudgil, K.D., E. Kim, O.J. Yun, H.H. Chi, E. Brahn, and E.E. Sercarz. Environmental modulation of autoimmune arthritis involves the spontaneous microbial induction of T cell responses to regulatory determinants within heat shock protein 65. J. Immunol. 2001, 166: 4237.
Moudgil, K.D. and E.E. Sercarz. The self-directed T cell repertoire: its creation and activation. Rev. Immunogenetics 2000, 2: 26.
Melo, M.E.F., K.D. Moudgil, and E.E. Sercarz. Autotolerance, In: Encyclopedia of Stress 2000: Vol. I, p. 284-290, Academic Press, San Diego, CA.
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