A photo of Chandrashekhar Pasare.

Professor, Division of Immunobiology


Biography & Affiliation


Dr. Pasare's laboratory is involved in studying the Toll-like receptor signaling pathway in cells of the innate immune system and also investigating the mechanisms by which these receptors regulate adaptive immune responses. Toll-like receptors are a major family of pattern recognition receptors of the innate immune systems and sense presence of bacterial, fungal and viral pathogens. Activation of these receptors leads to secretion of cytokines and chemokine that are important for protection against pathogens. However unregulated production of cytokines and chemokine leads to inflammation associated with both auto-inflammatory and auto-immune diseases. Work in the Pasare lab has led to novel insights into several aspects of both innate and adaptive immunity. His lab identified BCAP to be a novel adapter of the TLR signaling pathway and its importance in linking TLR signaling to PI3 Kinase activation and dampening of inflammatory responses. Work from his laboratory also led to discovery of a rapid NLRP3 inflammasome activation pathway this is specifically regulated by IRAK1. Work in his laboratory led to also identified a crucial role for IL-1R signaling in regulating effector function of CD4 T cells of all lineages. His current focus is to gain molecular understanding of inflammation and to tease out the complex cross-talk between innate and adaptive immune systems.

Research Interests

Innate immunity; toll-like receptor signaling; dendritic cell biology; innate control of adaptive immunity; regulation of inflammation


Immunobiology, Center for Inflammation and Tolerance


PhD: National Institute of Immunology, New Delhi, India, 2000.

Post Doctoral Fellowship: Immunobiology, Yale University School of Medicine, New Haven, CT, 2006.


Deason K, Troutman TD, Jain A, Challa DK, Mandraju R, Brewer T, Ward ES, Pasare C. BCAP links IL-1R to the PI3K-mTOR pathway and regulates pathogenic Th17 cell differentiation. J Exp Med. 2018 Aug 9.

Jain A, Song R, Wakeland EK, Pasare C. T cell-intrinsic IL-1R signaling licenses effector cytokine production by memory CD4 T cells. Nat Commun. 2018 Aug 9;9(1):3185.

Mandraju R, Jain A, Gao Y, Ouyang Z, Norgard MV, Pasare C. MyD88 Signaling in T Cells Is Critical for Effector CD4 T Cell Differentiation following a Transitional T Follicular Helper Cell Stage. Infect Immun. 2018 Apr 23;86(5).

Jain A, Pasare C. Innate Control of Adaptive Immunity: Beyond the Three-Signal Paradigm. J Immunol. 2017 May 15;198(10):3791-3800.

Akbar MA, Mandraju R, Tracy C, Hu W, Pasare C, Krämer H. ARC Syndrome-Linked Vps33B Protein Is Required for Inflammatory Endosomal Maturation and Signal Termination. Immunity. 2016 Aug 16;45(2):267-79.

Hu W, Jain A, Gao Y, Dozmorov IM, Mandraju R, Wakeland EK, Pasare C. Differential outcome of TRIF-mediated signaling in TLR4 and TLR3 induced DC maturation. Proc Natl Acad Sci U S A. 2015 Nov 10;112(45):13994-9

Mandraju R, Murray S, Forman J, Pasare C. Differential ability of surface and endosomal TLRs to induce CD8 T cell responses in vivo. J Immunol. 2014 May 1;192(9):4303-15.

Lin KM, Hu W, Troutman TD, Jennings M, Brewer T, Li X, Nanda S, Cohen P, Thomas JA, Pasare C. IRAK-1 bypasses priming and directly links TLRs to rapid NLRP3 inflammasome activation.
Proc Natl Acad Sci U S A. 2014 Jan 14;111(2):775-80.

Troutman TD, Hu W, Fulenchek S, Yamazaki T, Kurosaki T, Bazan JF, Pasare C. Role for B-cell adapter for PI3K (BCAP) as a signaling adapter linking Toll-like receptors (TLRs) to serine/threonine kinases PI3K/Akt. Proc Natl Acad Sci U S A. 2012 Jan 3;109(1):273-8.

Hu W, Troutman TD, Edukulla R, Pasare C. Priming microenvironments dictate cytokine requirements for T helper 17 cell lineage commitment. Immunity. 2011 Dec 23;35(6):1010-22.