An LKB1-mitochondria axis controls T_H17 effector function.

ABSTRACT: CD4⁺ T cell differentiation requires metabolic reprogramming to fulfil the bioenergetic demands of proliferation and effector function, and enforce specific transcriptional programmes^1-3. Mitochondrial membrane dynamics sustains mitochondrial processes⁴, including respiration and tricarboxylic acid (TCA) cycle metabolism⁵, but whether mitochondrial membrane remodelling orchestrates CD4⁺ T cell differentiation remains unclear. Here we show that unlike other CD4⁺ T cell subsets, T helper 17 (T_H17) cells have fused mitochondria with tight cristae. T cell-specific deletion of optic atrophy 1 (OPA1), which regulates inner mitochondrial membrane fusion and cristae morphology⁶, revealed that T_H17 ce

SUBMITTER: Baixauli F 

PROVIDER: S-EPMC9844518 | biostudies-literature | 2022 Oct

REPOSITORIES: biostudies-literature