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