CD4+ cells treated with DNA methylation inhibitors induce autologous B cell differentiation

Clin Immunol Immunopathol. 1990 Jun;55(3):368-81. doi: 10.1016/0090-1229(90)90125-a.

Abstract

The DNA methylation inhibitor 5-azacytidine induces autoreactivity in cloned CD4+ T cells, but the functional consequences of this response are unknown. We now report that CD4+ T cells treated with 5-azacytidine respond to autologous antigen-presenting cells and induce autologous B cell differentiation without exogenous antigen or mitogen. This mechanism could play a role in some autoimmune diseases characterized by T cell DNA hypomethylation and polyclonal B cell activation.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Acecainide / pharmacology
  • Antibody Formation / physiology
  • Antigen-Presenting Cells / immunology
  • Antigens, CD / biosynthesis
  • Antigens, Differentiation / biosynthesis
  • Azacitidine / pharmacology*
  • B-Lymphocytes / immunology*
  • CD4-Positive T-Lymphocytes / drug effects*
  • CD4-Positive T-Lymphocytes / immunology
  • Cell Differentiation / immunology
  • DNA / drug effects
  • Histocompatibility Antigens / biosynthesis
  • Humans
  • Hydroxyurea / pharmacology
  • Integrin beta1
  • Leukocyte Common Antigens
  • Methylation
  • Procainamide / pharmacology

Substances

  • Antigens, CD
  • Antigens, Differentiation
  • Histocompatibility Antigens
  • Integrin beta1
  • DNA
  • Acecainide
  • Leukocyte Common Antigens
  • Procainamide
  • Azacitidine
  • Hydroxyurea