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Resistance to tumor necrosis factor-alpha-induced apoptosis in human T-lymphotropic virus type I-infected T cell lines.
- Source :
-
AIDS research and human retroviruses [AIDS Res Hum Retroviruses] 2002 Feb 10; Vol. 18 (3), pp. 207-12. - Publication Year :
- 2002
-
Abstract
- Induction of apoptosis of virus-infected cells is an important host cell defense mechanism. It is well documented that T cells may undergo apoptosis due to interactions between Fas and Fas ligand (FasL). In addition, signals that induce apoptosis in T cells can result from interaction of tumor necrosis factor (TNF)-alpha with TNF receptors (TNFRs). It has been shown that human T cell lines expressing HTLV-I have decreased sensitivity to Fas-mediated apoptosis. The susceptibility of HTLV-I-infected cells to TNF-alpha-induced apoptosis remains to be elucidated. In the present study, we examined the expression of TNFRs on HTLV-I-infected T cell lines that expressed T-cell activation markers and thus phenotypically resemble activated T cells. Different from primary activated T cells that expressed both TNFRs, none of the five HTLV-I-infected T cell lines studied had detectable TNFR1 and only three had TNFR2 on their cell surfaces, although, the RNA transcripts of both TNFR genes could be detected via reverse transcription-polymerase chain reaction in these cell lines. The T cell blasts, which we activated in vitro, were sensitive to apoptosis induced by TNF-alpha and by antibodies to TNFR1 and/or TNFR2. However, all of the HTLV-I-infected cell lines expressing TNFR2 were resistant to TNF-alpha-mediated apoptosis. These findings suggest that HTLV-I infection may interfere with the autonomous suicide programs of T cells, not only Fas/FasL but also TNFRs/TNF-alpha pathways, to prolong the life of the infected cells. This may contribute to viral persistence and favor survival and subsequent expansion of dysregulated infected T cells with the potential to produce HTLV-I-associated autoimmune-like diseases or malignancies.
- Subjects :
- Antigens, CD metabolism
Cell Line
Drug Resistance
Humans
Receptors, Tumor Necrosis Factor metabolism
Receptors, Tumor Necrosis Factor, Type I
Receptors, Tumor Necrosis Factor, Type II
T-Lymphocytes drug effects
T-Lymphocytes metabolism
T-Lymphocytes pathology
Tumor Necrosis Factor-alpha pharmacology
Apoptosis
Human T-lymphotropic virus 1 physiology
T-Lymphocytes virology
Tumor Necrosis Factor-alpha metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 0889-2229
- Volume :
- 18
- Issue :
- 3
- Database :
- MEDLINE
- Journal :
- AIDS research and human retroviruses
- Publication Type :
- Academic Journal
- Accession number :
- 11839155
- Full Text :
- https://doi.org/10.1089/08892220252781266