The incidence of end-stage kidney disease is increasing worldwide and represents a major clinical and economic burden. Currently there are no effective treatments for this fatal condition. The kidney is an organ particularly susceptible to damage caused by infections and autoinflammatory conditions. Even so, renal immunology remains remarkably understudied by the immunologists. Over the past twelve years, the Biswas laboratory has successfully positioned itself to fulfill this important knowledge gap. Using mouse models and patients with kidney disease, the major goal of Biswas Laboratory is to understand the basic molecular and cellular mechanisms of kidney damage during autoinflammatory conditions and infections and utilize this knowledge for therapeutic benefit. Thus, research in the Biswas laboratory embodies the features of a basic scientist with scientific contributions spanning from very basic work in cell/animal models to more clinical work in humans.

The research in the Biswas Laboratory is divided into several areas, centered around understanding “organ-specific” immunological events in the kidney during infection and autoinflammatory conditions:

1. Determine how pathogenic inflammatory cytokine Interleukin-17 (IL-17) drives irreversible kidney damage, with the goal of revealing effective therapeutic approaches to block IL-17 signaling in chronic kidney diseases including lupus nephritis, ANCA vasculitis etc.
2. To define the mechanisms of IL-17-mediated renal immunity and immunometabolic regulation of neutrophil function against invasive candidiasis, methicillin-resistant S. aureus and uropathogenic E. coli infections. The data generated from these studies will inspire the development of effective vaccines against kidney infections caused by fungal and bacterial pathogens.
3. To determine the cellular and molecular mechanisms of renal fibrosis, the outcome of acute or chronic kidney diseases leading to kidney dysfunction.
4. To define why patients with kidney disease are unable to control infections, which is the second major cause of mortality in these patients. Using mouse models of end-stage kidney disease and dialysis patients, we systemically assess the innate, adaptive and mucosal immune dysfunction caused by uremic toxins.