Dr. Soumen Basak

A network of interconnected signaling pathways shapes cellular responses. The canonical and non-canonical NF-kB pathways represent two major immune-related cell signaling axes. In the Systems Immunology Laboratory (SIL), we combine biochemical, genetic, omics-based and computational approaches to investigate the role of these pathways – both individually and as components of the broader cellular network - in regulating immune functions in health and disease. As detailed below, we leverage pre-clinical mouse models and patient-derived samples to understand how NF-kB signaling instructs immune and metabolic reprogramming in the contexts of i) inflammation-associated ailments and ii) anti-viral immunity. We anticipate that insights from these cell-signaling studies may guide the development of improved therapeutic strategies in the future.  

1. Inflammation-associated ailments: The immune circuitry linking colitogenic or metabolic perturbations to intestinal barrier dysfunction and associated pathologies remains incompletely understood. Luminal microbial substances activate the canonical RelA NF-kB pathway, inducing the expression of inflammatory cytokines and chemokines. While controlled NF-kB signaling is important for effective innate immune responses, excessive RelA activity causes inflammatory tissue damage in the intestine. In a systems-modeling approach, we are developing a computational model of the NF-kB system to elucidate the regulatory circuitry governing its dynamical activity. Best known for its functions in secondary lymph nodes, lymphotoxin-b receptor also activates non-canonical RelB NF-kB in intestinal epithelial cells. We are integrating biochemical, genetic, immunological, transcriptomic, and metagenomic investigations involving pre-clinical mouse models and patient-derived samples to also define the role of epithelial non-canonical RelB NF-kB signaling in inflammatory bowel disease (IBD) and metabolic dysfunction-associated steatotic liver disease (MASLD).
2. Anti-viral immunity: Viral sensing by immune cells activates the canonical RelA NF-kB pathway as well as IRF transcription factors. While RelA-driven expression of cytokines and chemokines instructs CD8⁺ T cell engagement during viral pathogenesis, IRF3 upregulates type-1 interferons, a family of antiviral mediators. On the other hand, the non-canonical RelB NF-kB pathway restricts viral propagation in vivo by virtue of its ability to orchestrate secondary lymph node functions. In this program, we are addressing how these intracellular pathways interface in defining antiviral immunity. In particular, we are focusing on two important viruses of human health relevance – namely, Chandipura virus, a virus often associated with encephalitis outbreaks in India, and Chikungunya virus, a continuing global threat, particularly in the context of climate change. Combining ex vivo cell signaling studies and mouse models for viral infection, we are addressing how cell-signaling pathways modulate viral pathogenesis, and how viral-encoded factors subvert these host pathways.

Awards:
• 2026 JC Bose Grant from Anusandhan National Research Foundation.
• 2022 Elected as a Fellow of the Indian National Science Academy (INSA).
• 2021 Elected Fellow of the Indian Academy of Sciences (IASc).
• 2021 Elected Fellow of the National Academy of Sciences India (NASI).
• 2019 Received Shanti Swarup Bhatnagar Award for Research Excellence.
• 2018 Received National Bioscience Award for Career Development.
• 2017 Elected as a member of the Guha Research Conference.
• 2010-2015 Intermediate Fellow, Wellcome Trust-DBT India Alliance.

Collaborators:
G. Aneeshkumar, Santiswarup Singha and CL Meena, NII-New Delhi; James Gomes, Manidipa Banerjee and Tapan Nayak, IIT- Delhi; Abhyudai Singh, Univ. of Delaware; Vineet Ahuja from AIIMS-Delhi; Dr. Siddhesh Kamat, IISER-Pune; Amit Awasthi and Bhabatosh Das, THSTI-Faridabad; Nanaocha Sharma, Pardeep Bhardwaj, IBSD-Manipur.