The innate immune response to pathogens involves the expression and secretion of inflammatory cytokines that act to facilitate eradication of the infecting pathogen. The dysregulation of cytokine production (chronic inflammation) can have negative effects on the host. Therefore, a fundamental understanding of the molecular mechanisms regulating inflammation is essential for the development of therapeutic approaches for inflammatory disorders. We identify a novel role for the transcription factor GLI3 in regulating cytokine expression in response to TLR-TRIF signaling. GLI3 KO in monocytes induces a phenotype that indicates GLI3 associates with inflammatory pathways in response to TLR-TRIF stimulation. In this proposal, we will further elucidate the role of GLI3 in regulating cytokine expression in monocytes and explore the relevance of this regulation in inflammatory responses.

Agency
National Institute of Health (NIH)
Institute
National Institute of General Medical Sciences (NIGMS)
Type
Exploratory Grants (P20)
Project #
5P20GM113131-04
Application #
10176697
Study Section
Special Emphasis Panel (ZGM1)
Program Officer
Bernal, Federico
Project Start
Project End
Budget Start
2020-06-01
Budget End
2021-05-31
Support Year
4
Fiscal Year
2020
Total Cost
Indirect Cost
Name
University of New Hampshire
Department
Type
DUNS #
111089470
City
Durham
State
NH
Country
United States
Zip Code
03824
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