Partha Sarathi Biswas, MVSc, PhD
Office: Dept. of Medicine, Div. of Rheumatology
Lab: 725 BST-South
Pittsburgh, PA 15261
- Bachelor of Veterinary Sciences, WBUAFS, India, 1998
- Master of Veterinary Sciences, CCSHAU, India, 2000
- PhD, Comparative and Experimental Medicine, The University of Tennessee, USA, 2005
- Associate Professor, Department of Medicine
- Associate Professor, Department of Immunology
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.
Pubmed link: https://www.ncbi.nlm.nih.gov/pubmed/?term=Biswas+ps
- 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] (Highlighted in Nature Reviews Nephrology)
- Ramani K., Tan R.J., Zhou D., Coleman B.M., Jawale C.V., Liu Y and Biswas P.S. (2018). IL-17 Receptor Signaling Negatively Regulates the Development of Tubulointerstitial Fibrosis in the Kidney. Mediators Inflamm. 2018;2018:5103672. doi: 10.1155/2018/5103672. [PMID: 30405230]
- Biswas P.S*. (2018). IL-17 in renal immunity and autoimmunity. J Immunol. Aug;120: 282-288. [PMID: 30772195]
- Ramani K., Garg A.V., Jawale C.V., Conti H. R., Whibley N., Jackson E. K., Shiva S. S., Kolls J. K., Gaffen S. L. and Biswas P.S. (2016). The Kallikrein-kinin System: a Novel Mediator of IL-17-driven Anti-Candida Immunity in the Kidney. Plos Pathogens. Nov 4;12(11):e1005952. doi: 10.1371/journal.ppat.1005952. [PMID: 27814401] (Recommended in F1000Prime as being of special significance in its field by F1000 Faculty Member Neil Andrew Robert Gow)
- Biswas P.S*., Agarwal R., Levesque M., Maers K. and Ramani K. (2015). Type I Interferon and T helper 17 cells co-exist and co-regulate disease pathogenesis in lupus patients. International J. Rheum. Dis. 18(6):646-53. [PMID: 25960196]
- Ramani K., Pawaria S., Maers K. Huppler A.R., Gaffen S.L. and Biswas P.S. (2014). An essential role of interleukin-17 receptor signaling in the development of autoimmune glomerulonephritis. J. Leukoc. Biol. 96(3):463-72. [PMID: 24935958] (Most frequently downloaded manuscript from J. Leokocyte Biology in first six months after publication)
- Pawaria S., Ramani K., Maers K., Liu Y., Kane L., Levesque M. and Biswas P.S. (2014). Complement component C5a permits the coexistence of pathogenic Th17 cells and type I IFN in lupus. J. Immunol. 193(7):3288-95. [PMID: 25149466] (Featured in the “In this Issue” section of J. Immunology, 193(7):3179-82)