International Immunology, Vol 9, 1303-1310, Copyright © 1997 by Oxford University Press
K Oda, H Asao, M Higuchi, N Tanaka, S Moffatt, M Nakamura, K Tabayashi and K Sugamura
Our previous study demonstrated that IL-2 suppressed growth of human T cell
lines, in which the suppression was observed with members among
HTLV-I-infected T cell lines independent of IL-2 for growth. In this study,
we examined the molecular mechanism of IL-2-induced growth suppression with
two HTLV-I-infected T cell lines; TL-OmI expressing endogenously three
subunits, i.e. alpha, beta and gamma chains, of the IL-2 receptor, and an
MT-1 transfectant expressing the endogenous alpha and gamma chains and
exogenous beta chain. Our analysis revealed that IL-2 induced apoptosis in
both T cell lines. Experiments with inhibitors for the proteases
responsible for apoptosis signals showed that caspase 1 (IL-1
beta-converting enzyme) was not involved in apoptosis induced by IL-2.
Other MT-1 sublines introduced with mutant beta chains demonstrated that
IL-2-induced apoptosis required signals from both the serine-rich (S)
region and acidic (A) region of the IL-2 receptor beta chain, which are
essential but not critical for IL-2- mediated cell growth respectively.
Collectively, IL-2 functions not only on growth promotion and prevention of
apoptosis but also on induction of apoptosis, which may be implicated in
physiological regulation of immune reactions by controlling growth and
activation of T cells.
ARTICLES
Induction of IL-1 beta-converting enzyme-independent apoptosis by IL-2 in human T cell lines
Department of Microbiology, Tohoku University School of Medicine, Sendai, Japan.
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  P. Hu, M. Mizokami, G. Ruoff, L. A. Khawli, and A. L. Epstein Generation of low-toxicity interleukin-2 fusion proteins devoid of vasopermeability activity Blood, June 15, 2003; 101(12): 4853 - 4861. [Abstract] [Full Text] [PDF]
|
|