Abstract
Originalsprog | Engelsk |
---|---|
Tidsskrift | Cytokine |
Vol/bind | 10 |
Udgave nummer | 9 |
Sider (fra-til) | 662-8 |
Antal sider | 6 |
ISSN | 1043-4666 |
DOI | |
Status | Udgivet - 1998 |
Bibliografisk note
Copyright 1998 Academic Press.Adgang til dokumentet
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The role of caspase 3 and BclxL in the action of interleukin 7 (IL-7): a survival factor in activated human T cells. / Amos, C L; Woetmann, A; Nielsen, M; Geisler, C; Odum, N; Brown, B. L.; Dobson, P R.
I: Cytokine, Bind 10, Nr. 9, 1998, s. 662-8.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review
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TY - JOUR
T1 - The role of caspase 3 and BclxL in the action of interleukin 7 (IL-7): a survival factor in activated human T cells
AU - Amos, C L
AU - Woetmann, A
AU - Nielsen, M
AU - Geisler, C
AU - Odum, N
AU - Brown, B. L.
AU - Dobson, P R
N1 - Keywords: Apoptosis; Caspase 3; Caspases; Cell Survival; Cells, Cultured; Dexamethasone; Enzyme Activation; Gene Expression Regulation; Glucocorticoids; Humans; Interleukin-2; Interleukin-7; Lymphocyte Activation; Poly(ADP-ribose) Polymerases; Proto-Oncogene Proteins c-bcl-2; T-Lymphocytes; bcl-X Protein
PY - 1998
Y1 - 1998
N2 - The effects of interleukin 7 (IL-7) on apoptosis in interleukin 2 (IL-2)-dependent, activated, primary, human T lymphocytes (hT cells) was examined. IL-7 (like IL-2) rescued cells from apoptosis, as measured by their cellular DNA profile and fragmentation. IL-2 also acted as a mitogen in these T cells. Both cytokines abrogated the dexamethasone-induced stimulation of Caspase 3 and prevented the cleavage of poly (ADP-ribose) polymerase (PARP), a substrate for the Caspase 3. IL-7 upregulated the expression of Bc1xL and counteracted the downregulation of this anti-apoptotic protein by the synthetic glucocorticoid, dexamethasone. Bcl-2 protein expression was uupregulated by IL-7 with or without dexamethasone, but Bc1-2 was expressed at a much lower level than BclxL in these cells. Levels of Bax did not markedly change on either cytokine stimulation or dexamethasone treatment. An unidentified 23-kDa band, which was recognized by the anti-Bc1-2 antibody, was induced by dexamthasone and suppressed by IL-7 and IL-2. This protein was subject to independent regulation as compared to the p26 Bc1-2 protein, suggesting that it may be a novel factor, possibly involved in the regulation of apoptosis. A clear role for IL-7 as a survival factor for cytokine withdrawal and glucocorticoid induced apoptosis in activated primary hT cells is implicated. In addition, regulation of BclxL and downstream inhibition of Caspase 3 activity may mediate this rescue signal.
AB - The effects of interleukin 7 (IL-7) on apoptosis in interleukin 2 (IL-2)-dependent, activated, primary, human T lymphocytes (hT cells) was examined. IL-7 (like IL-2) rescued cells from apoptosis, as measured by their cellular DNA profile and fragmentation. IL-2 also acted as a mitogen in these T cells. Both cytokines abrogated the dexamethasone-induced stimulation of Caspase 3 and prevented the cleavage of poly (ADP-ribose) polymerase (PARP), a substrate for the Caspase 3. IL-7 upregulated the expression of Bc1xL and counteracted the downregulation of this anti-apoptotic protein by the synthetic glucocorticoid, dexamethasone. Bcl-2 protein expression was uupregulated by IL-7 with or without dexamethasone, but Bc1-2 was expressed at a much lower level than BclxL in these cells. Levels of Bax did not markedly change on either cytokine stimulation or dexamethasone treatment. An unidentified 23-kDa band, which was recognized by the anti-Bc1-2 antibody, was induced by dexamthasone and suppressed by IL-7 and IL-2. This protein was subject to independent regulation as compared to the p26 Bc1-2 protein, suggesting that it may be a novel factor, possibly involved in the regulation of apoptosis. A clear role for IL-7 as a survival factor for cytokine withdrawal and glucocorticoid induced apoptosis in activated primary hT cells is implicated. In addition, regulation of BclxL and downstream inhibition of Caspase 3 activity may mediate this rescue signal.
U2 - 10.1006/cyto.1998.0351
DO - 10.1006/cyto.1998.0351
M3 - Journal article
C2 - 9770327
VL - 10
SP - 662
EP - 668
JO - Cytokine
JF - Cytokine
SN - 1043-4666
IS - 9
ER -