Microbiology and Immunology
Howard Hall, 320
(410) 706-7804 (office)
(410) 706-7918 (lab)
Education and Training
Doctoral education: All India Institute of Medical Science, New Delhi, India
Postdoctoral training: Gillis W. Long Hansen's Disease Center, Carville, LA
Postdoctoral training: University of California at Los Angeles (UCLA), Los Angeles, CA
I have developed and led a focused and productive research program in autoimmunity and immune regulation. My studies are based on the rat adjuvant arthritis (AA) model of human rheumatoid arthritis and the mouse/rat experimental autoimmune encephalomyelitis (EAE) model of human multiple sclerosis. In AA, my research projects are focused on: a) the immunological basis of susceptibility/ resistance to arthritis of defined inbred rat strains of the same MHC haplotype; b) the influence of environmental factors (the housing environment, exposure to nicotine/ tobacco smoke, etc.) on the initiation, progression, and regression of autoimmune arthritis; c) the dynamics of cytokine responses and their cross-regulation during the course of arthritis; d) the factors influencing the target organ (the joint) susceptibility in autoimmune arthritis; e) the role of T helper 17 (Th17) and Foxp3+ regulatory T cells (Treg) in the pathogenesis of arthritis; f) the development of novel immunomodulatory and therapeutic approaches for arthritis, including the use of natural products as well as the use of joint-homing peptides for targeted drug delivery into inflamed joints. In EAE, my research is aimed at: a) the identification of peptide ligands that preferentially home to the inflamed spinal cord and/or brain in mice; and b) the use of such peptides for targeted therapy of EAE. Over the years, my research work has been funded by the NIH through R01, R21, R03, P01 (sub-project), P50 (sub-project) grants; by the Arthritis Foundation, Atlanta, GA and the Rheumatology Research Foundation, Atlanta, GA; and by the Baltimore Veterans Affairs Medical Center, Baltimore through VA Merit. I have trained over 20 doctoral students and postdoctoral fellows, including NIH F31-, F32-, and T32-supported trainees, and an equal number of undergraduate students in research. For the past 11 years, I have served as the section head for the immunology section of Host Defenses and Infectious Diseases (HDID) course for medical students. I have published over 125 research papers and review articles.
Immunology, Autoimmunity, Arthritis, Multiple Sclerosis, Immune Regulation, Heat-shock Proteins, Antigen Processing and Presentation, Natural products, Herbal Medicine
Langan D, Kim EY, Moudgil KD. Modulation of autoimmune arthritis by environmental 'hygiene' and commensal microbiota. Cell Immunol. 2019; 339: 59-67.
Meka RR, Venkatesha SH, Moudgil KD. Peptide-directed liposomal delivery improves the therapeutic index of an immunomodulatory cytokine in controlling autoimmune arthritis. J. Control. Release 2018; 286: 279-288.
Dudics S, Venkatesha SH, Moudgil KD. The Micro-RNA expression profiles of autoimmune arthritis reveal novel biomarkers of the disease and therapeutic response. Int. J. Mol. Sci. 2018; 19.pii: E2293.
Kim EK, Moudgil KD. Immunomodulation of autoimmune arthritis by pro-inflammatory cytokines. Cytokine 2017; 98: 87-96.
Venkatesha SH, Dudics S, Astry B, Moudgil KD. Control of autoimmune inflammation by celastrol, a natural triterpenoid. Pathog. Dis. 2016, 74(6): pii. ftw029.
Meka RR, Venkatesha SH, Dudics S, Acharya B, Moudgil KD. IL-27-induced modulation of autoimmunity and its therapeutic potential. Autoimmun Rev.2015, 14: 1131-41.
Astry B, Venkatesha SH, Laurence A, Christensen-Quick A, Garzino-Demo A, Frieman MB, O'Shea JJ, Moudgil KD. Celastrol, a Chinese herbal compound, controls autoimmune inflammation by altering the balance of pathogenic and regulatory T cells in the target organ. Clin Immunol. 2015, 157: 228-38.
Yang Y-H, Rajaiah R, Ruoslahti E, and Moudgil, KD. Peptides targeting inflamed synovial vasculature attenuate autoimmune arthritis. Proc. Natl. Acad. Sci. USA 2011, 108: 12857.
Rajaiah R, Puttabyatappa M, Polumuri SK, Moudgil KD. Interleukin-27 and interferon-gamma are involved in regulation of autoimmune arthritis.J Biol Chem. 2011;286(4):2817.
Nanjundaiah SM, Venkatesha SH, Yu H, Tong L, Stains JP, Moudgil KD. Celastrus and its bioactive Celastrol protect against bone damage in autoimmune arthritis by modulating the osteo-immune crosstalk. J Biol Chem. 2012, 287: 22216.
Venkatesha SH, Yu H, Rajaiah R, Tong L, Moudgil KD. Celastrus-derived celastrol suppresses autoimmune arthritis by modulating antigen-induced cellular and humoral effector responses. J Biol Chem. 2011;286(17):15138.
Moudgil, K.D. and M. Durai. Regulation of autoimmune arthritis by self heat-shock proteins. Trends. Immunol. 2008, 29: 412.
Meka RR, Venkatesha SH, Acharya B, Moudgil KD. Peptide-targeted liposomal delivery of dexamethasone for arthritis therapy. Nanomedicine (Lond). 2019 ;14(11):1455-1469.
Venkatesha SH, Moudgil KD. Celastrol suppresses experimental autoimmune encephalomyelitis via MAPK/SGK1-regulated mediators of autoimmune pathology. Inflamm Res. 2019;68(4):285-296.
Venkatesha SH, Dudics S, Song Y, Mahurkar A, Moudgil KD. The miRNA Expression Profile of Experimental Autoimmune Encephalomyelitis Reveals Novel Potential Disease Biomarkers. Int J Mol Sci. 2018;19(12). pii: E3990.
Dudics S, Langan D, Meka RR, Venkatesha SH, Berman BM, Che CT, Moudgil KD. Natural Products for the Treatmenmune Arthritis: Their Mechanisms of Action, Targeted Delivery, and Interplay with the Host Microbiome. Int J Mol Sci. 2018;19(9). pii: E2508.
Venkatesha SH, Dudics S, Weingartner E, So EC, Pedra J, Moudgil KD. Altered Th17/Treg balance and dysregulated IL-1ß response influence susceptibility/resistance to experimental autoimmune arthritis. Int J Immunopathol Pharmacol. 2015, 28: 318-28.
Venkatesha SH, Dudics S, Acharya B, Moudgil KD. Cytokine-Modulating Strategies and Newer Cytokine Targets for Arthritis Therapy. Int J Mol Sci. 2014;16: 887-906.
Tong L, Nanjundaiah SM, Venkatesha SH, Astry B, Yu H, Moudgil KD. Pristimerin, a naturally occurring triterpenoid, protects against autoimmune arthritis by modulating the cellular and soluble immune mediators of inflammation and tissue damage. Clin Immunol. 2014;155:220-30.
Moudgil KD, Berman BM. Traditional Chinese medicine: potential for clinical treatment of rheumatoid arthritis. Expert Rev Clin Immunol. 2014,12:1-4.
Yu H, Lu C, Tan MT, Moudgil KD. Comparative antigen-induced gene expression profiles unveil novel aspects of susceptibility/resistance to adjuvant arthritis in rats. Mol Immunol. 2013, 56(4):531-539.
Moudgil KD, Thompson SJ, Geraci F, De Paepe B, Shoenfeld Y. Heat-shock proteins in autoimmunity. Autoimmune Dis. 2013, 2013: 621417.
Yu H, Yang YH, Rajaiah R, Moudgil KD. Nicotine-induced differential modulation of autoimmune arthritis in the Lewis rat involves changes in interleukin-17 and anti-cyclic citrullinated peptide antibodies. Arthritis Rheum. 2011 Apr;63(4):981. doi: 10.1002/art.30219.
Huang M.N., H. Yu and K.D. Moudgil. The involvement of heat-shock proteins in the pathogenesis of autoimmune arthritis: a critical appraisal.Semin. Arthritis Rheum. 2010:40: 164.
Rajaiah R. and K.D. Moudgil. Heat-shock protein can promote as well as regulate autoimmunity. Autoimmun. Rev. 2009, 8: 388.
Satpute S.R., R. Rajaiah, S.K. Polumuri and K.D. Moudgil. Tolerization with Hsp65 induces protection against adjuvant-induced arthritis by modulating the antigen-directed interferon-gamma, interleukin-17 and antibody responses. Arthritis Rheum. 2009, 60: 103.
Kim E.K. and K.D. Moudgil. The determinants of susceptibility/resistance to adjuvant arthritis in rats. Arthritis Res. Therapy 2009, 11(4): 239.
Durai M., M.N. Huang, and K.D. Moudgil. Self heat-shock protein 65-mediated regulation of autoimmune arthritis. J. Autoimmun. 2009 Oct 1. [Epub ahead of print].
Rajaiah R., D.Y. Lee, Z. Ma, A.Y. Fan, L. Lao, H.H. Fong, B.M. Berman, and K.D. Moudgil. Huo-Luo-Xiao-Ling Dan modulates antigen-directed immune response in adjuvant-induced inflammation. J. Ethnopharmacol. 2009, 123(1): 40.
Rajaiah, R., Y. Yang, S.R. Satpute, M. Durai, and K.D. Moudgil. Immunopathogenesis and Treatment of Autoimmune Arthritis in Animal Models, In: Recent Research Developments on Rheumatic Diseases (edited by Antonio La Cava, MD, PhD, UCLA, Los Angeles, CA, USA), Research Signpost Publishers, 2009, Ch. 1.
Mia M.Y., E.Y. Kim, S.R. Satpute, and K.D. Moudgil. The Dynamics of Articular Leukocyte Trafficking and the Immune Response to Self Heat-Shock Protein 65 Influence Arthritis Susceptibility. J. Clin. Immunol. 2008, 28: 420.
Kim E.Y., H.H. Chi, R. Rajaiah, and K.D. Moudgil. Exogenous tumor necrosis factor-alpha induces suppression of autoimmune arthritis.Arthritis Res. Ther. 2008, 10: R38.
Kim, E.Y., H.H. Chi, M. Bouziane, A. Gaur, and K.D. Moudgil. Regulation of autoimmune arthritis by the pro-inflammatory cytokine interferon-gamma. Clin. Immunol. 2008, 127: 98-106.
Kim E. and K. D. Moudgil. Regulation of autoimmune inflammation by pro-inflammatory cytokines. Immunol. Lett. 2008, 120: 1.
Satpute, S.R., M. Durai, K.D. Moudgil. Antigen-Specific Tolerogenic and Immunomodulatory Strategies for the treatment of Autoimmune Arthritis. Semin Arthritis Rheum 2008, 38(3):195.
Kim H. R., R. Rajaiah, Q-L Wu, S. R. Satpute, M. T. Tan, J. E. Simon, B. M. Berman, and K. D. Moudgil. Green tea affords protection against autoimmune arthritis in rats by modulating the disease-related immune events. J. Nutrition 2008, 138: 2111.
Coelho, V., F. Broere, R. J. Binder, Y. Shoenfeld, and K.D. Moudgil. Heat-shock proteins: pro-inflammatory versus regulatory attributes. Cell Stress Chaperones 2008, 13: 119.
Rajaiah R. and K.D. Moudgil. Animal Models, In: Rheumatoid Arthritis (eds. M.C. Hochberg, A.J. Silman, J.S. Smolen, M.H. Weisman, and M.E. Weinblatt), Mosby, Inc., an affiliate of Elsevier, Inc., 2008, Ch. 8N.
Satpute, S., N. Soukhareva, D.W. Scott, and K.D. Moudgil. Mycobacterial hsp65-IgG-expressing tolerogenic B cells induce protection against adjuvant arthritis in the Lewis rat. Arthritis and Rheumatism 2007, 56: 1490.
Durai, M., H.R. Kim, K. Bala, and K.D. Moudgil. T Cells Against the Pathogenic and Protective Epitopes of Heat-shock Protein 65 Are Crossreactive and Display Functional Similarity: Novel Aspect of Regulation of Autoimmune Arthritis. J. Rheumatol 2007, 34: 2134.
Tong, L. and K.D. Moudgil. Celastrus aculeatus Merr. suppresses the induction and progression of autoimmune arthritis by modulating immune response to heat-shock protein 65. Arthritis Res. Therapy 2007, 9: R70.
Sinha, P., J.A. Snyder, E. Y. Kim, and K. D. Moudgil. The Major Histocompatibility Complex Haplotypes Dictate and the Background Genes Fine-tune the Dominant versus the Cryptic Response Profile of a T-cell Determinant within a Native Antigen: Relevance to Disease Susceptibility and Vaccination. Scand. J. Immunol. 2007, 65: 158.
Kim, H. R., E. Y. Kim, J. Cerny, and K. D. Moudgil. Antibody responses to mycobacterial and self heat-shock protein 65 in autoimmune arthritis: epitope specificity and implication in pathogenesis. J. Immunol. 2006, 177: 6634.
Jiang, X. and K. D. Moudgil. 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. 2006, 63: 338.
Bala K. K. and K. D. Moudgil. Induction and maintenance of self tolerance: the role of CD4+CD25+ regulatory T cells. Arch. Immunol. Ther. Exp. 2006, 54: 307.
Zhu, H., K. Liu, J. Cerny, T. Imoto, and K. D. Moudgil. 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 2005, 175: 2252.
Mia, M. Y., M. Durai, H. R. Kim, and K. D. Moudgil. Heat shock protein 65-reactive T cells are involved in the pathogenesis of non-antigenic dimethyl dioctadecyl ammonium bromide-induced arthritis. J Immunol 2005, 175: 219.
Moudgil, K. D., and E. E. Sercarz. Understanding crypticity is the key to revealing the pathogenesis of autoimmunity. Trends Immunol 2005, 26:355.
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
Antigen Processing and Presentation
Induction and Regulation of Autoimmunity
Targeted drug delivery in autoimmune diseases
Herbal therapy of autoimmune diseases
Secondary appointment: Division of Rheumatology, Department of Medicine, School of Medicine, UMB