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Protection Against Type 1 Diabetes Development in Mice With 4E-BP2 Deletion.
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ABSTRACT: Article highlights
Mammalian target of rapamycin complex 1 (mTORC1) signaling is essential to β-cell mass, function, and adaptive immunity; however, its specific downstream mediators in type 1 diabetes (T1D) remain poorly defined. We investigated eukaryotic translation initiation factor 4E-binding protein 2 (4E-BP2), a major translational regulator downstream of mTORC1, by using global 4E-BP2-knockout mice on the NOD background. Loss of 4E-BP2 protected male NOD mice from T1D through preservation of β-cell mass and function, coupled with attenuation of autoimmune responses. These findings identify 4E-BP2 as a novel immunometabolic node, highlighting its potential as a therapeutic target for T1D prevention and treatment.
SUBMITTER: Pita-Grisanti V
PROVIDER: S-EPMC12823344 | biostudies-literature | 2026 Jan
REPOSITORIES: biostudies-literature
Publications
Protection Against Type 1 Diabetes Development in Mice With 4E-BP2 Deletion.
Diabetes 20260101 2
Type 1 diabetes (T1D) is an autoimmune disease characterized by β-cell destruction promoted by autoreactive T cells. Eukaryotic translation initiation factor 4E (eIF4E)–binding protein 1 (4E-BP1) and 4E-BP2 are translational repressors and downstream targets of mammalian target of rapamycin complex 1 (mTORC1). Activation of the 4E-BP2/eIF4E pathway by 4E-BP2 deletion promotes translation initiation, inducing β-cell expansion and proliferation and regulating adaptive immunity. However, the involv ...[more]