Lymphocyte function-associated antigen 1 overexpression and T cell autoreactivity.
OBJECTIVE
To determine if DNA methylation inhibitors make T cells autoreactive by inducing lymphocyte function-associated antigen type 1 (LFA-1) (CD11a/CD18) overexpression.


METHODS
T cell clones were treated with 3 distinct DNA methylation inhibitors or were stably transfected with a CD18 cDNA in a mammalian expression vector, and the effects on LFA-1 expression and activation requirements were examined.


RESULTS
LFA-1 overexpression, caused by DNA methylation inhibitors or by transfection, correlates with the development of autoreactivity.


CONCLUSIONS
LFA-1 overexpression may contribute to T cell autoreactivity.
Richardson
B
B
University of Michigan, Ann Arbor.
Powers
D
D
Hooper
F
F
Yung
R L
RL
O'Rourke
K
K
D001374:Azacitidine / Q000494:pharmacology; D018821:CD18 Antigens / Q000235:genetics; D004247:DNA / Q000378:metabolism; D018076:DNA, Complementary; D006801:Humans; D008213:Lymphocyte Activation; D016169:Lymphocyte Function-Associated Antigen-1 / Q000378:metabolism*; D008745:Methylation / Q000187:drug effects; D010957:Plasmids / Q000502:physiology; D011342:Procainamide / Q000494:pharmacology; D013601:T-Lymphocytes / Q000187:drug effects / Q000502:physiology* / Q000528:radiation effects; D014162:Transfection; D014466:Ultraviolet Rays
D018821:CD18 Antigens; D018076:DNA, Complementary; D016169:Lymphocyte Function-Associated Antigen-1; D004247:DNA; D011342:Procainamide; D001374:Azacitidine