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The susceptibility to Fas-mediated apoptosis was evaluated in seven T-cell lines (two infected with HTLV-2, one with HTLV-1, and four HTLV-free) as well as in Jurkat cells transfected with a Tax-2 expressing vector. Fas-mediated apoptosis was significantly reduced in the HTLV-1- and HTLV-2-infected lines in comparison with the HTLV-free lines regardless of the surface expression of Fas antigen (which was no different in the infected and uninfected cells). Fas-mediated apoptosis was also significantly inhibited in Jurkat cells transfected with the Tax-2 expressing vector without any modification in Fas expression. There was significantly more antiapoptotic Bcl-x(L) mRNA and protein in the transfected than in the untransfected Jurkat T cells. In conclusion, our results suggest that HTLV-2 is capable of inhibiting Fas-mediated apoptosis by means of a mechanism involving the tax-2 gene and probably the expression of bcl-x(L) messenger and protein.
Bcl-XL, T-Lymphocytes, Blotting, Western, bcl-X Protein, Apoptosis, Transfection, Antibodies, Jurkat Cells, Virology, Proto-Oncogene Proteins, In Situ Nick-End Labeling, Humans, RNA, Messenger, fas Receptor, tax protein, programmed cell death, Cells, Cultured, bcl-2-Associated X Protein, Human T-lymphotropic virus 1, Human T-lymphotropic virus 2, Gene Products, tax, HTLV-2 pathogenesis, Proto-Oncogene Proteins c-bcl-2, Culture Media, Conditioned, HTLV-II Infections, human retroviruses, Bcl-XL; HTLV-2 pathogenesis; Human retroviruses; Programmed cell death; Tax protein
Bcl-XL, T-Lymphocytes, Blotting, Western, bcl-X Protein, Apoptosis, Transfection, Antibodies, Jurkat Cells, Virology, Proto-Oncogene Proteins, In Situ Nick-End Labeling, Humans, RNA, Messenger, fas Receptor, tax protein, programmed cell death, Cells, Cultured, bcl-2-Associated X Protein, Human T-lymphotropic virus 1, Human T-lymphotropic virus 2, Gene Products, tax, HTLV-2 pathogenesis, Proto-Oncogene Proteins c-bcl-2, Culture Media, Conditioned, HTLV-II Infections, human retroviruses, Bcl-XL; HTLV-2 pathogenesis; Human retroviruses; Programmed cell death; Tax protein
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