Selective degradation of PU.1 during autophagy represses the differentiation and antitumour activity of T_H9 cells.

ABSTRACT: Autophagy, a catabolic mechanism that involves degradation of cellular components, is essential for cell homeostasis. Although autophagy favours the lineage stability of regulatory T cells, the contribution of autophagy to the differentiation of effector CD4 T cells remains unclear. Here we show that autophagy selectively represses T helper 9 (T_H9) cell differentiation. CD4 T cells lacking Atg3 or Atg5 have increased interleukin-9 (IL-9) expression upon differentiation into T_H9 cells relative to Atg3- or Atg5-expressing control cells. In addition, the T_H9 cell transcription factor, PU.1, undergoes K63 ubiquitination and degradation through p62-dependent selective autophagy. Finally, the blockade of autophagy enhances T_H9 cell anticancer functions

SUBMITTER: Rivera Vargas T 

PROVIDER: S-EPMC5602674 | biostudies-literature | 2017 Sep

REPOSITORIES: biostudies-literature