Ddb1 Is Essential for the Expansion of CD4+ Helper T Cells by Regulating Cell Cycle Progression and Cell Death

Front Immunol. 2021 Aug 30:12:722273. doi: 10.3389/fimmu.2021.722273. eCollection 2021.

Abstract

Follicular helper T (TFH) cells are specialized CD4+ helper T cells that provide help to B cells in humoral immunity. However, the molecular mechanism underlying generation of TFH cells is incompletely understood. Here, we reported that Damage-specific DNA binding protein 1 (Ddb1) was required for expansion of CD4+ helper T cells including TFH and Th1 cells, germinal center response, and antibody response to acute viral infection. Ddb1 deficiency in activated CD4+ T cells resulted in cell cycle arrest at G2-M phase and increased cell death, due to accumulation of DNA damage and hyperactivation of ATM/ATR-Chk1 signaling. Moreover, mice with deletion of both Cul4a and Cul4b in activated CD4+ T cells phenocopied Ddb1-deficient mice, suggesting that E3 ligase-dependent function of Ddb1 was crucial for genome maintenance and helper T-cell generation. Therefore, our results indicate that Ddb1 is an essential positive regulator in the expansion of CD4+ helper T cells.

Keywords: DNA damage response; Ddb1; G2/M arrest; T cell differentiation; Th1; follicular helper T cells; humoral immunity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Cycle / genetics*
  • Cell Cycle Checkpoints
  • Cell Death
  • Cell Differentiation / genetics
  • Cell Differentiation / immunology
  • DNA Damage
  • DNA-Binding Proteins / genetics*
  • Gene Expression
  • Homeostasis
  • Immunophenotyping
  • Lymphocyte Activation / genetics*
  • Lymphocyte Activation / immunology*
  • Mice
  • Mice, Knockout
  • T-Lymphocyte Subsets / immunology
  • T-Lymphocyte Subsets / metabolism
  • T-Lymphocytes, Helper-Inducer / immunology
  • T-Lymphocytes, Helper-Inducer / metabolism*
  • Tumor Suppressor Protein p53 / metabolism

Substances

  • DNA-Binding Proteins
  • Ddb1 protein, mouse
  • Tumor Suppressor Protein p53