Lack of phospho-eIF4E worsens experimental colitis by inhibiting Treg suppressive activity.

ABSTRACT:

Background

Phosphorylation of eIF4E by MNK1/2 modulates protein synthesis by controlling the translation of specific mRNAs. Immune cells use the MNK1/2-eIF4E axis to adapt their gene expression in response to environmental cues, but its dysregulated activity promotes disease progression. While recent examples using cancer models have identified CD8⁺ T-cells as a conduit for the tumor-supporting role of the MNK1/2-eIF4E axis, the impact of phospho-eIF4E on CD4⁺ T-cell subsets, specifically regulatory T-cells, remains unclear. To fill this knowledge gap, we studied the impact of phospho-eIF4E-deficiency on Treg activity in mice in an inflammatory context using a model of murine colitis and in human PBMCs.

Results

We found that Tregs isolated from mice def

SUBMITTER: Santinon F 

PROVIDER: S-EPMC12593924 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature