Dipankar Nandi

Department of Biochemistry
Research Areas: 
Studying novel microbial genes during stress and infection, Understanding the host encoded immune responses
Research Highlights: 

The long-term objective our laboratory is to understand biological responses to different stimuli. For this purpose, we utilize microbial systems as well as the host encoded immune system. Over the years, we have established a diverse array of models and expertise that help us to understand the roles of various genes and signals in modulating microbial and host encoded responses. Overall, our laboratory works at the interface of microbiology and immunology. Broadly, the twin areas of interests of our laboratory are: (1) Studying novel microbial genes during stress and infection - Several years back, our laboratory identified Peptidase N (PepN), the sole M1 family member in E. coli and S. typhimurium to be a major aminopeptidase. Over the years, we have studied the roles of this enzyme during stress and infection, using a combination of genetics, microbiology, biochemistry and immunology. Ongoing research involves studying some aspects of the structure-function relationship of PepN with respect to its biochemistry and function. We are also investigating the roles of other proteases and peptidases during stress responses. However, the emphasis now will be on the functional roles of novel genes during stress responses and infections. (2) Understanding the host encoded immune responses - We are pursuing two aspects of research under this broad category: (a) T cell biology: T cells are required for cellular immunity and play key roles during the adaptive immune response. Efforts are geared towards studying the mechanistic aspects, especially the roles of different species of free radicals, in affecting T cell responses. In addition, we are studying the roles of small molecules in modulating CD4+ T cell activation and survival and attempting to understand their mechanism/s of action. As far as in vivo T cell responses are concerned, we have shown the role of heat killed Mycobacterium indicus prannii (an adjuvant) in inducing anti-tumor T cells to reduce tumor growth. We have also standardized a model of thymic atrophy using a model of oral infection by Salmonella enterica serovar Typhimurium, an intracellular pathogen. We are studying multiple aspects during this process, including, expression of cell surface markers, death markers, the roles of different signalling pathways etc. The mechanistic insights uncovered in this study may be important in designing effective strategies to reduce thymic atrophy during infections and boost host responses. (b) Inflammatory and Interferon-gamma modulated responses: A key cytokine involved in inflammatory immune responses is Interferon-gamma (IFN-gamma) which is produced mainly by activated T cells and NK cells. Our laboratory has shown the roles of oxidative and nitrosative stress in modulating the expression of IFN-gamma-regulated genes. We have now extended this study to macrophages and are attempting to identify novel IFN-gamma regulated genes and responses that are modulated by Nos2. Current efforts are also directed towards understanding the expression and roles of novel IFN-gamma-regulated genes in cell growth suppression and modulation of intracellular growth of Salmonella enterica serovar Typhimurium.