Common γ -chain cytokine signaling is required for macroautophagy induction during CD4+ T-cell activation

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

Macroautophagy is a cellular process that mediates degradation in the lysosome of cytoplasmic components including proteins and organelles. Previous studies have shown that macroautophagy is induced in activated T cells to regulate organelle homeostasis and the cell’s energy metabolism. However, the signaling pathways that initiate and regulate activation-induced macroautophagy in T cells have not been identified. Here, we show that activation-induced macroautophagy in T cells depends on signaling from common γ -chain cytokines. Consequently, inhibition of signaling through JAK3, induced downstream of cytokine receptors containing the common γ -chain, prevents full induction of macroautophagy in activated T cells. Moreover, we found that common γ -chain cytokines are not only required for macroautophagy upregulation during T cell activation but can themselves induce macroautophagy. Our data also show that macroautophagy induction in T cells is associated with an increase of LC3 expression that is mediated by a posttranscriptional mechanism. Overall, our findings unveiled a new role for common γ -chain cytokines as a molecular link between autophagy induction and T-cell activation.

Original languageEnglish (US)
Pages (from-to)1864-1877
Number of pages14
JournalAutophagy
Volume11
Issue number10
DOIs
StatePublished - 2015

Fingerprint

Autophagy
Cytokines
T-Lymphocytes
Organelles
Cytokine Receptors
Lysosomes
Energy Metabolism
Homeostasis
Up-Regulation

Keywords

  • Common γ -chain
  • Interleukin 2
  • JAK
  • Macroautophagy
  • T cell

ASJC Scopus subject areas

  • Cell Biology
  • Molecular Biology

Cite this

Common γ -chain cytokine signaling is required for macroautophagy induction during CD4+ T-cell activation. / Botbol, Yair M.; Patel, Bindi; Macian-Juan, Fernando.

In: Autophagy, Vol. 11, No. 10, 2015, p. 1864-1877.

Research output: Contribution to journalArticle

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