期刊
ELIFE
卷 4, 期 -, 页码 -出版社
ELIFE SCIENCES PUBLICATIONS LTD
DOI: 10.7554/eLife.08698
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资金
- National Health and Medical NHMRC Elizabeth Carola G Vinuesa Research Council Blackburn Fellowship
- National Health and Medical Research Council NHMRC Elizabeth Blackburn Fellowship
- National Health and Medical Research Council NHMRC Senior Principle Research Fellowship
- National Health and Medical Research Council NHMRC Career Development Fellowship
- National Health and Medical Research Council NHMRC Project [APP1061580]
- National Health and Medical Research Council NHMRC Program [APP1016953]
T follicular helper cells (Tfh) are critical for the longevity and quality of antibody mediated protection against infection. Yet few signaling pathways have been identified to be unique solely to Tfh development. ROQUIN is a post-transcriptional repressor of T cells, acting through its ROQ domain to destabilize mRNA targets important for Thl, Th17, and Tfh biology. Here, we report that ROQUIN has a paradoxical function on Tfh differentiation mediated by its RING domain: mice with a T cell-specific deletion of the ROQUIN RING domain have unchanged Thl, Th2, Th17, and Tregs during a T-dependent response but show a profoundly defective antigen-specific Tfh compartment. ROQUIN RING signaling directly antagonized the catalytic al subunit of adenosine monophosphate-activated protein kinase (AMPK), a central stress-responsive regulator of cellular metabolism and mTOR signaling, which is known to facilitate T-dependent humoral immunity. We therefore unexpectedly uncover a ROQUIN AMPK metabolic signaling nexus essential for selectively promoting Tfh responses.
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