Open AccessPhenotypic and functional similarities between 5‐azacytidine‐treated t cells and a t cell subset in patients with active systemic lupus erythematosus
Author(s) -
Richardson Bruce C.,
Strahler John R.,
Pivirotto T. Scott,
Quddus Jawaid,
Bayliss Garry E.,
Gross Laura A.,
O'Rourke Kenneth S.,
Powers Daniel,
Hanash Samir M.,
Johnson Marcia A.
Publication year - 1992
Publication title -
arthritis & rheumatism
Language(s) - English
Resource type - Journals
eISSN - 1529-0131
pISSN - 0004-3591
DOI - 10.1002/art.1780350608
Subject(s) - dna methylation , immunology , phenotype , cd11a , antigen , lupus erythematosus , biology , t cell , gene , autoimmunity , gene expression , microbiology and biotechnology , antibody , integrin alpha m , flow cytometry , immune system , genetics , cd18
Objective. Antigen‐specific CD4+ T cells treated with DNA methylation inhibitors become autoreactive, suggesting a novel mechanism for autoimmunity. To test whether this mechanism might be involved in systemic lupus erythematosus (SLE), phenotypic markers for the autoreactive cells were sought. Methods. Cloned normal T cells were treated with the DNA methylation inhibitor 5‐azacytidine (5‐azaC) and studied for altered gene expression. T cells from patients with active SLE were then studied for a similar change in gene expression, and cells expressing the marker were tested for autoreactivity. Results. 5‐azaC‐treated normal T cells had increased CD11a (leukocyte function‐associated antigen 1α) expression relative to other membrane molecules. A T cell subset with similar CD11a expression was found in patients with active SLE. This subset contained cells that spontaneously lysed autologous macrophages, with a specificity similar to that of 5‐azaC‐treated cells. Conclusion. The model of 5‐azaC‐induced autoreactivity may have relevance to SLE.