Journal
IMMUNITY
Volume 43, Issue 4, Pages 690-702Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2015.08.017
Keywords
-
Categories
Funding
- National Science Foundation Graduate Research Fellowship Program [2012099695]
- NIH [F32AI094791, AR40072, AR062842, AI075157, AR053495, AR063942]
- Alliance for Lupus Research
Ask authors/readers for more resources
The differentiation of CD4(+) helper T cell subsets with diverse effector functions is accompanied by changes in metabolism required to meet their bioenergetic demands. We find that follicular B helper T (Tfh) cells exhibited less proliferation, glycolysis, and mitochondrial respiration, accompanied by reduced mTOR kinase activity compared to T helper 1 (Th1) cells in response to acute viral infection. IL-2-mediated activation of the Akt kinase and mTORc1 signaling was both necessary and sufficient to shift differentiation away from Tfh cells, instead promoting that of Th1 cells. These findings were not the result of generalized signaling attenuation in Tfh cells, because they retained the ability to flux calcium and activate NFAT-transcription-factor-dependent cytokine production. These data identify the interleukin-2 (IL-2)-mTORc1 axis as a critical orchestrator of the reciprocal balance between Tfh and Th1 cell fates and their respective metabolic activities after acute viral infection.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available