Abstract：
:CD4(+) T cells differentiate into phenotypically distinct T helper cells upon antigenic stimulation. Regulation of plasticity between these CD4(+) T-cell lineages is critical for immune homeostasis and prevention of autoimmune disease. However, the factors that regulate lineage stability are largely unknown. Here we investigate a role for retinoic acid (RA) in the regulation of lineage stability using T helper 1 (Th1) cells, traditionally considered the most phenotypically stable Th subset. We found that RA, through its receptor RARα, sustains stable expression of Th1 lineage specifying genes, as well as repressing genes that instruct Th17-cell fate. RA signaling is essential for limiting Th1-cell conversion into Th17 effectors and for preventing pathogenic Th17 responses in vivo. Our study identifies RA-RARα as a key component of the regulatory network governing maintenance and plasticity of Th1-cell fate and defines an additional pathway for the development of Th17 cells.
journal_name
Immunityjournal_title
Immunityauthors
Brown CC,Esterhazy D,Sarde A,London M,Pullabhatla V,Osma-Garcia I,Al-Bader R,Ortiz C,Elgueta R,Arno M,de Rinaldis E,Mucida D,Lord GM,Noelle RJdoi
10.1016/j.immuni.2015.02.003subject
Has Abstractpub_date
2015-03-17 00:00:00pages
499-511issue
3eissn
1074-7613issn
1097-4180pii
S1074-7613(15)00078-3journal_volume
42pub_type
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