Open AccessRole of tumor necrosis factor‐α and glucocorticoid on lipopolysaccharide (LPS)‐induced apoptosis of thymocytes
Author(s) -
Kato Y.,
Morikawa A.,
Sugiyama T.,
Koide N.,
Jiang GZ.,
Takahashi K.,
Yokochi T.
Publication year - 1995
Publication title -
fems immunology & medical microbiology
Language(s) - English
Resource type - Journals
eISSN - 1574-695X
pISSN - 0928-8244
DOI - 10.1111/j.1574-695x.1995.tb00192.x
Subject(s) - tumor necrosis factor alpha , apoptosis , lipopolysaccharide , thymocyte , glucocorticoid , biology , in vivo , endocrinology , in vitro , glucocorticoid receptor , medicine , necrosis , immunology , t cell , immune system , biochemistry , microbiology and biotechnology
Administration of bacterial lipopolysaccharide (LPS) into mice markedly induced the apoptosis of CD4 + 8 + thymocytes. The injection of anti‐tumor necrosis factor (TNF)‐α antibody or RU38486, a glucocorticoid receptor antagonist, into mice definitely inhibited LPS‐induced apoptosis of thymocytes. Addition of the sera 1 h after injection of LPS into in vitro cultures of thymocytes caused thymocyte apoptosis. It was also prevented by either anti‐TNF‐α antibody or RU38486. Further, recombinant TNF‐α and hydrocortisone collaborated in induction of the thymocyte apoptosis in vitro. The in vivo phenomenon of LPS‐induced apoptosis of thymocytes was reproducible by the in vitro experimental system. It was therefore suggested that both TNF‐α and glucocorticoid participate and collaborate as effector molecules in LPS‐induced apoptosis of thymocytes.