How We're Keeping You Safe | What Patients & Families Need to Know
Member, Division of Immunobiology
Professor, UC Department of Pediatrics
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.
Innate immunity; toll-like receptor signaling; dendritic cell biology; innate control of adaptive immunity; regulation of inflammation
Immunobiology, Inflammation and Tolerance
Chandrashekhar Pasare, DVM, PhD5/5/2020
Chandrashekhar Pasare, DVM, PhD12/17/2019
PhD: National Institute of Immunology, New Delhi, India, 2000.
Post Doctoral Fellowship: Immunobiology, Yale University School of Medicine, New Haven, CT, 2006.
IRAK1 is a critical mediator of inflammation-induced preterm birth.
Jain, VG; Kong, F; Kallapur, SG; Presicce, P; Senthamaraikannnan, P; Cappelletti, M; Chougnet, CA; Bhattacharyya, S; Pasare, C; Muglia, LJ.
Journal of immunology (Baltimore, Md. : 1950).
Suppression of Inflammasome Activation by IRF8 and IRF4 in cDCs Is Critical for T Cell Priming.
McDaniel, MM; Kottyan, LC; Singh, H; Pasare, C.
Transcriptional profiling identifies caspase-1 as a T cell–intrinsic regulator of Th17 differentiation.
Gao, Y; Deason, K; Jain, A; Irizarry-Caro, RA; Dozmorov, I; Coughlin, LA; Rauch, I; Evers, BM; Koh, AY; Wakeland, EK; et al.
The Journal of Experimental Medicine.
Allergen-Induced C5a/C5aR1 Axis Activation in Pulmonary CD11b(+) cDCs Promotes Pulmonary Tolerance through Downregulation of CD40.
Antoniou, K; Ender, F; Vollbrandt, T; Laumonnier, Y; Rathmann, F; Pasare, C; Singh, H; Koehl, J.
T cells instruct myeloid cells to produce inflammasome-independent IL-1β and cause autoimmunity.
Jain, A; Irizarry-Caro, RA; McDaniel, MM; Chawla, AS; Carroll, KR; Overcast, GR; Philip, NH; Oberst, A; Chervonsky, AV; Katz, JD; et al.
An autophagy-inducing and TLR-2 activating BCG vaccine induces a robust protection against tuberculosis in mice.
Khan, A; Bakhru, P; Saikolappan, S; Das, K; Soudani, E; Singh, CR; Estrella, JL; Zhang, D; Pasare, C; Ma, Y; et al.
T cell-intrinsic IL-1R signaling licenses effector cytokine production by memory CD4 T cells.
Jain, A; Song, R; Wakeland, EK; Pasare, C.
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.
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.
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.
3333 Burnet Avenue, Cincinnati, Ohio 45229-3026 | 1-513-636-4200 | 1-800-344-2462
© 1999-2020 Cincinnati Children's Hospital Medical Center. All rights reserved.