Steroid nuclear receptor coactivators in T cell differentiation

NIH RePORTER · NIH · R01 · $510,194 · view on reporter.nih.gov ↗

Abstract

In human, uncontrolled pathogenic responses of IL-17+ cells are linked to various autoimmunity such as multiple sclerosis, Colitis and even autism whereas defective IL-17+ cells impairs protective immunity against infection by bacteria and fungus. IL-17 is produced from both adaptive Th17 cells and innate lymphocytes that contribute to immune responses at different phases. Effective control of the scale of Th17 responses is thus critical for treatment of above immune dysfunction. SRC1 and SRC3 are the functional co-factors for RORt, the essential transcription factor controlling Th17 function. Currently, poor understanding of the mechanisms responsible for the function of these co-factors prevents the development of potent clinical treatments to boost protective Th17 immunity against infection and repress pathogenic immunity responsible for autoimmunity. The objective of this proposal is to determine the role of SRC1 and SRC3 in the regulation of T cell-mediated immunity. Our proposed study will lay the foundation for understanding the fundamental role of SRC1 and SRC3 in adaptive T cells and innate lymphocytes, which will facilitate the development of specific and effective immunomodulatory therapies to boost protective immunity and suppress pathogenic IL-17+ cell- mediated autoimmunity.

Key facts

NIH application ID
9858214
Project number
5R01AI109644-07
Recipient
BECKMAN RESEARCH INSTITUTE/CITY OF HOPE
Principal Investigator
Zuoming Sun
Activity code
R01
Funding institute
NIH
Fiscal year
2020
Award amount
$510,194
Award type
5
Project period
2014-05-01 → 2024-04-30