Umesh  Deshmukh Degree(s): PhD Graduate School: National Institute of Immunology, New Delhi Primary Appointment: Associate Professor, Medicine, Nephrology Research Interests: Activation of Innate and Adaptive Immunity by Microbiota and it's role in autoimmune disorders. Email Address: usd7w@Virginia.EDU

Research Description

My laboratory is interested in investigating pathogenetic mechanisms of rheumatic autoimmune disorders, Systemic Lupus Erythematosus and Sjögren’s syndrome. While lupus is a multi organ disorder involving kidneys, skin, lungs and heart; Sjögren’s syndrome mainly affects the exocrine glands causing the dry eye and dry mouth symptoms. A common feature of both diseases is activation of self-reactive T and B cells, and generation of anti-nuclear autoantibodies. Recent literature clearly indicates that normal microbiota shapes an individuals immune repertoire.

Currently the major emphasis of our research is on understanding how oral and gut microbiota contribute towards the initiation and amplification of autoimmune responses in Lupus and Sjögren’s syndrome. In addition to basic research, my laboratory also has a strong translational focus. In this regard, we are exploring the feasibility of therapeutic agents targeting GPCRs for treatment of autoimmunity and restoration organ function.

Selected Publications

Jiang C, US Deshmukh, F Gaskin, H Bagavant, J Hanson, CS David, SM Fu. 2010. Differential responses to Smith D autoantigen by mice with HLA-DR and HLA-DQ transgenes: dominant responses by HLA-DR3 transgenic mice with diversification of autoantibodies to small nuclear ribonucleoprotein, double-stranded DNA, and nuclear antigens. J Immunol. 184:1085-91

Davis Sim, H Bagavant, YM Scindia, Y Ge, F Gaskin, SM Fu, US Deshmukh. 2009. Genetic complementation leading to augmented autoantibody responses to lupus-associated small nuclear ribonucleoprotein complex. J Immunol. 183: 3505-3511.

Sharma R, US Deshmukh, L Zheng, SM Fu, and S-T Ju. 2009. X-linked Foxp3 (Sf) mutation dominantly inhibits submandibular gland development and inflammation respectively by adaptive and innate immune mechanisms. J. Immunol. 183: 3212-3218.

Deshmukh US, SR Nandula, PR Thimmalapura, YM Scindia and H Bagavant. 2009. Activation of innate immune responses through toll-like receptor 3 causes a rapid loss of salivary gland function. J Oral Pathol Med, 38(1):42-47.