A photo of Chandrashekhar Pasare.

Member, Division of Immunobiology

Professor, UC Department of Pediatrics

513-636-6656

Biography & Affiliation

Biography

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

Academic Affiliation

Professor, UC Department of Pediatrics

Departments

Immunobiology, Inflammation and Tolerance

Education

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

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

Publications

T cell-intrinsic IL-1R signaling licenses effector cytokine production by memory CD4 T cells. Jain, A; Song, R; Wakeland, EK; Pasare, C. Nature Communications. 2018; 9.

Regulation of contact sensitivity in non-obese diabetic (NOD) mice by innate immunity. Szczepanik, M; Majewska-Szczepanik, M; Wong, FS; Kowalczyk, P; Pasare, C; Wen, L. Contact Dermatitis. 2018; 79:197-207.

BCAP links IL-1R to the PI3K-mTOR pathway and regulates pathogenic Th17 cell differentiation. Deason, K; Troutman, TD; Jain, A; Challa, DK; Mandraju, R; Brewer, T; Ward, ES; Pasare, C. The Journal of Experimental Medicine. 2018; 215:2413-2428.

MyD88 Signaling in T Cells Is Critical for Effector CD4 T Cell Differentiation following a Transitional T Follicular Helper Cell Stage. Mandraju, R; Jain, A; Gao, Y; Ouyang, Z; Norgard, MV; Pasare, C. Infection and Immunity. 2018; 86.

Inhibition of IRAK1 Ubiquitination Determines Glucocorticoid Sensitivity for TLR9-Induced Inflammation in Macrophages. Kong, F; Liu, Z; Jain, VG; Shima, K; Suzuki, T; Muglia, LJ; Starczynowski, DT; Pasare, C; Bhattacharyya, S. Journal of immunology (Baltimore, Md. : 1950). 2017; 199:3654-3667.

Innate Control of Adaptive Immunity: Beyond the Three-Signal Paradigm. Jain, A; Pasare, C. Journal of immunology (Baltimore, Md. : 1950). 2017; 198:3791-3800.

ARC Syndrome-Linked Vps33B Protein Is Required for Inflammatory Endosomal Maturation and Signal Termination. Akbar, MA; Mandraju, R; Tracy, C; Hu, W; Pasare, C; Kramer, H. Immunity. 2016; 45:267-279.

Regulatory polymorphisms modulate the expression of HLA class II molecules and promote autoimmunity. Raj, P; Rai, E; Song, R; Khan, S; Wakeland, BE; Viswanathan, K; Arana, C; Liang, C; Zhang, B; Dozmorov, I; et al. eLife. 2016; 5.

Comprehensive RNAi-based screening of human and mouse TLR pathways identifies species-specific preferences in signaling protein use. Sun, J; Li, N; Oh, K; Dutta, B; Vayttaden, SJ; Lin, B; Ebert, TS; De Nardo, D; Davis, J; Bagirzadeh, R; et al. Science Signaling. 2016; 9.

The DNA Sensor AIM2 Maintains Intestinal Homeostasis via Regulation of Epithelial Antimicrobial Host Defense. Hu, S; Peng, L; Kwak, Y; Tekippe, EM; Pasare, C; Malter, JS; Hooper, LV; Zaki, MH. Cell Reports. 2015; 13:1922-1936.