Partha Sarathi Biswas, DVM, PhD

  • Associate Professor, Department of Medicine, Division of Rheumatology and Clinical Immunology
  • Associate Professor, Department of Immunology
  • Member, Graduate Program in Microbiology and Immunology (PMI)

Education & Training

  • PhD, Comparative and Experimental Medicine, University of Tennessee, 2005
  • Master of Veterinary Sciences, CCSHAU (India), 2000
  • Bachelor of Veterinary Sciences, WBUAFS (India), 1998

Research Interest Summary

Kidney Immunology, Infection, Immunity, Autoimmunity, IL-17, Renal Disease

Research Interests

The kidney is often subject to irreversible damage caused by infections and auto-inflammatory conditions. The incidence of end-stage kidney damage is increasing worldwide and represents a major clinical and economic burden and currently there are no effective treatments for this fatal condition. The complex inflammatory cytokine network and renal inflammatory events that drives the progression of kidney injury to irreversible damage is poorly understood. The research program in Biswas lab is divided into several areas, centered on cytokine Interleukin-17 (IL-17) signaling in the kidney. IL-17 is important for host defense against bacterial and fungal infections, but also implicated in tissue pathology if not regulated. We take advantage of multiple in vivo mouse models of acute and chronic kidney diseases and human bio-specimens to address the following questions mentioned below. Our long term goal is to reduce the morbidity and mortality associated with end-stage renal diseases caused by infections and auto-inflammatory conditions in the kidney.

1) Determine how IL-17 drives irreversible kidney damage, with the ultimate goal of revealing effective therapeutic approaches to block IL-17 signaling in chronic kidney diseases.

2) Delineate the mechanisms of IL-17-mediated renal immunity against disseminated candidiasis and uropathogenic E. coli infection. The data generated from these studies will inspire the development of effective vaccines against kidney infections caused by fungal and bacterial pathogens.

3) Define the role of IL-17 signaling in renal fibrosis, the final outcome of acute or chronic kidney diseases leading to kidney dysfunction.

4) Define the mechanisms of increased mortality in patients with kidney disease due to systemic bacterial and fungal infections.


Li D., Jawale C.V., Zhou C., Lin L., Trevejo-Nunez G.J., Rahman S.A., Mullet S.J., Das J., Wendell S.G., Delgoffe G.M., Lionakis M.S., Gaffen S.L. and Biswas P.S*. (2022). Fungal sensing leads to increased glycolysis of neutrophils by selectively regulating antifungal Glut1 activity. Cell Host & Microbe. In Press36.

Jawale C.V., Ramani K., Li D., Coleman B.M., Oberoi R.S., Kupul S., Lin l., Desai, J.V., Delgoffe, G.M., Lionakis M.S., Bender, F.H., Prokopienko A.J., Nolin, T.D., Gaffen S.L. and Biswas P.S*. (2020). Restoring glucose uptake rescues neutrophil dysfunction and protects against systemic fungal infection in mouse model of kidney disease. Sci. Trans. Med. 2020 Jun 17;12(548):eaay5691. doi: 10.1126/scitranslmed.aay5691. PMID: 325547038.

Li D.D., Bechara R., Ramani K., Jawale C.V., Li Y., Kolls J.K., Gaffen S.L*. and Biswas P.S*. (2021). RTEC-intrinsic IL-17-driven inflammatory circuit amplifies antibody-induced glomerulonephritis and is constrained by Regnase-1. JCI Insight. 8;6(13):e147505. doi: 10.1172/jci.insight.147505. PMID: 3423604937.

Jawale C.V., Li D.D., Ramani K., Lin L., Li K., Methe B. and Biswas P.S*. (2021). Uremia Coupled with Mucosal Damage Predisposes Mice with Kidney Disease to Systemic Infection by Commensal Candida albicans. Immunohorizons 15;5(1):16-24. doi: 10.4049/immunohorizons.2000114. PMID: 3345198832.

Ramani K., Jawale C.V., Verma A.H., Coleman B.M., Kolls J.K. and Biswas P.S*. (2018). Unexpected kidney-restricted role for IL-17 receptor signaling in defense against systemic Candida albicans infection. JCI Insight. 2018;3(9):e98241. 10.1172/jci.insight.98241. PMID: 29720566

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