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Optimal CD8+ T cell effector function requires costimulation-induced RNA-binding proteins that reprogram the

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Area of Science:

  • Immunology
  • Molecular Biology
  • Cellular Biology

Background:

  • T cell activation is critical for anti-cancer and anti-viral immunity.
  • Costimulation enhances T cell potency but its mechanisms remain unclear.
  • Current understanding emphasizes transcriptional control of T cell activation.

Purpose of the Study:

  • To investigate the role of post-transcriptional regulation in T cell costimulation.
  • To identify key molecular pathways and factors involved in costimulation-induced T cell reprogramming.
  • To explore novel therapeutic strategies for optimizing T cell activity.

Main Methods:

  • Analyzed T cells stimulated with CD134/CD137 costimulators.
  • Utilized RNA-sequencing (RNA-seq) to identify differential splicing and polyadenylation events.
  • Employed in vivo mouse and in vitro human models to study RNA-binding protein Tardbp function.

Main Results:

  • The spliceosome was the most enriched pathway in costimulated T cells.
  • Costimulation led to increased expression of 29 RNA-binding proteins and over 1000 differential RNA processing events.
  • Tardbp deficiency impaired effector cytokine production, T cell expansion, and isoform regulation.

Conclusions:

  • Post-transcriptional regulation via the spliceosome is a key mechanism in T cell costimulation.
  • RNA-binding protein Tardbp is essential for effective T cell responses.
  • Reprogramming mRNA isoform production presents a novel avenue for immunotherapy.