A photo of Chandrashekhar Pasare.

Chandrashekhar Pasare, DVM, PhD

  • Member, Division of Immunobiology
  • Professor, UC Department of Pediatrics



In my research, I pursue topics such as regulation of inflammation, dendritic cell biology, innate immunity, toll-like receptor signaling and the cross-talk between the innate and adaptive immune systems. Our lab’s primary goals are to understand how the innate and adaptive immune system interact with each other and to define the molecules that are part of this interaction.

We are also studying how inflammation is prompted by microbial recognition and during autoimmunity. In general, our objectives are 1) to obtain a molecular understanding of inflammation to develop new treatments for reducing autoimmunity and inflammation and 2) to define the complex communication between innate and adaptive immune systems in order to improve the design of vaccines.

Some of the most notable discoveries my colleagues and I have made include:

  • Discovering a completely new pathway for inflammation in which auto-reactive T cells guide the innate immune system to produce IL-1beta; the new pathway may be used to treat auto-immunity
  • Finding a new Toll-Like Receptor signaling adapter known as BCAP that reduces inflammation

My lab concentrates on identifying the innate immune system's main activation mechanisms and its effect on inflammation and adaptive immunity. The innate immune system depends on certain receptors known as pattern recognition receptors to distinguish pathogens.

Pathogen recognition via the innate immune system causes inflammation as well as adaptive immunity activation. One of my lab's major objectives is to identify the elaborate interaction and signaling between the innate and adaptive immune systems. My colleagues and I are specifically pursuing how the innate immune system prompts inflammation and how it affects both protective immunity and inflammatory conditions.

My research interests began due to my fascination with learning how the body’s immune system knows not to react to self but recognizes and responds to the microbial non-self. Our research has defined multiple new proteins and pathways in cells within innate and adaptive immune systems. We have utilized them as handles to direct questions regarding protective immunity, cancer and inflammatory diseases. We employ cutting-edge in vitro and in vivo methods in our research that may bring new targets to treat auto-immunity, cancer and inflammatory conditions.

I have more than twenty years of experience in the field of immunology and first began working at the Cincinnati Children’s Hospital Medical Center in 2018. My research has been published in numerous journals, including Nature, Science, Immunity, The Journal of Experimental Medicine, Nature Immunology, Cell Reports, Journal of Immunology and Nature Communications.


Effector memory CD4+ T cells induce damaging innate inflammation and autoimmune pathology by engaging CD40 and TNFR on myeloid cells. McDaniel, MM; Chawla, AS; Jain, A; Meibers, HE; Saha, I; Gao, Y; Jain, V; Roskin, K; Way, SS; Pasare, C. Science Immunology. 2022; 7.

Innate control of adaptive immunity and adaptive instruction of innate immunity: bi-directional flow of information. McDaniel, MM; Meibers, HE; Pasare, C. Current Opinion in Immunology. 2021; 73:25-33.

Environmental allergens trigger type 2 inflammation through ripoptosome activation. Brusilovsky, M; Rochman, M; Rochman, Y; Caldwell, JM; Mack, LE; Felton, JM; Habel, JE; Porollo, A; Pasare, C; Rothenberg, ME. Nature Immunology. 2021; 22:1316-1326.

IRF1 governs the differential interferon-stimulated gene responses in human monocytes and macrophages by regulating chromatin accessibility. Song, R; Gao, Y; Dozmorov, I; Malladi, V; Saha, I; McDaniel, MM; Parameswaran, S; Liang, C; Arana, C; Zhang, B; et al. Cell Reports. 2021; 34.

TLR signaling adapter BCAP regulates inflammatory to reparatory macrophage transition by promoting histone lactylation. Irizarry-Caro, RA; McDaniel, MM; Overcast, GR; Jain, VG; Troutman, TD; Pasare, C. Proceedings of the National Academy of Sciences of the United States of America. 2020; 117:30628-30638.

Deep sequencing reveals a DAP1 regulatory haplotype that potentiates autoimmunity in systemic lupus erythematosus. Raj, P; Song, R; Zhu, H; Riediger, L; Jun, DJ; Liang, C; Arana, C; Zhang, B; Gao, Y; Wakeland, BE; et al. Genome Biology. 2020; 21.

Hypersensitivity of Vps33B mutant flies to non-pathogenic infections is dictated by aberrant activation of p38b MAP kinase. Zhang, J; Tracy, C; Pasare, C; Zeng, J; Kraemer, H. Traffic. 2020; 21:578-589.

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. 2020; 204:2651-2660.

Suppression of Inflammasome Activation by IRF8 and IRF4 in cDCs Is Critical for T Cell Priming. McDaniel, MM; Kottyan, LC; Singh, H; Pasare, C. Cell Reports. 2020; 31.

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. Journal of Experimental Medicine. 2020; 217.

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