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Elife. 2018 May 31;7. pii: e33057. doi: 10.7554/eLife.33057.

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

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Laboratory of Molecular Neuro-Oncology, Howard Hughes Medical Institute, The Rockefeller University, New York, United States.
New York Genome Center, New York, United States.
Howard Hughes Medical Institute, Ludwig Center at Memorial Sloan Kettering Cancer Center, New York, United States.


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.


HITS-CLIP; RNA binding protein; T cell; anti-viral immunity; chromosomes; gene expression; immunology; inflammation; mouse; translation

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