Journal article
Attenuation of AMPK signaling by ROQUIN promotes T follicular helper cell formation
RR Ramiscal, IA Parish, RS Lee-Young, JJ Babon, J Blagih, A Pratama, J Martin, N Hawley, JY Cappello, PF Nieto, JI Ellyard, NJ Kershaw, RA Sweet, CC Goodnow, RG Jones, MA Febbraio, CG Vinuesa, V Athanasopoulos
Elife | ELIFE SCIENCES PUBLICATIONS LTD | Published : 2015
DOI: 10.7554/eLife.08698
Abstract
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 Th1, 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 Th1, Th2, Th17, and Tregs during a T-dependent response but show a profoundly defective antigen-specific Tfh compartment. ROQUIN RING signaling d..
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Awarded by National Health and Medical Research Council
Funding Acknowledgements
[ "Funder Grant reference number Author", "National Health and Medical Research Council NHMRC Elizabeth Blackburn Fellowship Carola G Vinuesa", "National Health and Medical Research Council NHMRC Senior Principle Research Fellowship Mark A Febbraio", "National Health and Medical Research Council NHMRC Career Development Fellowship Robert S Lee-Young", "National Health and Medical Research Council NHMRC Project Grant APP1061580 Carola G Vinuesa", "National Health and Medical Research Council NHMRC Program Grant APP1016953 Carola G Vinuesa", "The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication." ]