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Publication

ZFP36 RNA-binding proteins restrain T cell activation and anti-viral immunity.

eLife | 2018

Dynamic post-transcriptional control of RNA expression by RNA-binding proteins (RBPs) is critical during immune response. ZFP36 RBPs are prominent inflammatory regulators linked to autoimmunity and cancer, but functions in adaptive immunity are less clear. We used HITS-CLIP to define ZFP36 targets in mouse T cells, revealing unanticipated actions in regulating T-cell activation, proliferation, and effector functions. Transcriptome and ribosome profiling showed that ZFP36 represses mRNA target abundance and translation, notably through novel AU-rich sites in coding sequence. Functional studies revealed that ZFP36 regulates early T-cell activation kinetics cell autonomously, by attenuating activation marker expression, limiting T cell expansion, and promoting apoptosis. Strikingly, loss of ZFP36 in vivo accelerated T cell responses to acute viral infection and enhanced anti-viral immunity. These findings uncover a critical role for ZFP36 RBPs in restraining T cell expansion and effector functions, and suggest ZFP36 inhibition as a strategy to enhance immune-based therapies.

Pubmed ID: 29848443 RIS Download

Research resources used in this publication

HEK293T (RRID:CVCL_0063) (cell line)

Additional research tools detected in this publication

Antibodies used in this publication

Associated grants

Agency: NINDS NIH HHS, United States
Id: R01 NS081706
Agency: NIH HHS, United States
Id: R35NS097404
Agency: Howard Hughes Medical Institute, United States
Agency: NIH HHS, United States
Id: NS081706
Agency: NCI NIH HHS, United States
Id: P30 CA008748
Agency: NINDS NIH HHS, United States
Id: R35 NS097404
Agency: NINDS NIH HHS, United States
Id: R56 NS034389
Agency: NINDS NIH HHS, United States
Id: R01 NS034389
Agency: NIH HHS, United States
Id: NS034389

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