title: Resistance to Fas-mediated apoptosis of human T-cell lines expressing human T-lymphotropic virus type-2 (HTLV-2) Tax protein.
abstract: 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.
authors.affiliation: Istituto di Malattie Infettive e Tropicali, Università degli Studi di Milano, 20100 Milano, Italy. zehender@mailserver.unimi.it
authors.forename: G
authors.initials: G
authors.lastname: Zehender
authors.forename: S
authors.initials: S
authors.lastname: Varchetta
authors.forename: C
authors.initials: C
authors.lastname: De Maddalena
authors.forename: C
authors.initials: C
authors.lastname: Colasante
authors.forename: A
authors.initials: A
authors.lastname: Riva
authors.forename: L
authors.initials: L
authors.lastname: Meroni
authors.forename: M
authors.initials: M
authors.lastname: Moroni
authors.forename: M
authors.initials: M
authors.lastname: Galli
mesh_terms: D000906:Antibodies / Q000276:immunology / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects; D015153:Blotting, Western; D002478:Cells, Cultured; D017077:Culture Media, Conditioned / Q000494:pharmacology; D016356:Gene Products, tax / Q000235:genetics / Q000378:metabolism* / Q000494:pharmacology; D015491:HTLV-II Infections / Q000473:pathology / Q000821:virology; D015368:Human T-lymphotropic virus 1 / Q000235:genetics / Q000502:physiology; D015367:Human T-lymphotropic virus 2 / Q000235:genetics / Q000502:physiology*; D006801:Humans; D020287:In Situ Nick-End Labeling; D019169:Jurkat Cells; D011518:Proto-Oncogene Proteins / Q000235:genetics / Q000378:metabolism; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D013601:T-Lymphocytes / Q000187:drug effects / Q000378:metabolism / Q000473:pathology* / Q000821:virology*; D014162:Transfection; D051028:bcl-2-Associated X Protein; D051020:bcl-X Protein; D019014:fas Receptor / Q000032:analysis / Q000276:immunology / Q000502:physiology*
chemical_list: D000906:Antibodies; C494811:BCL2L1 protein, human; D017077:Culture Media, Conditioned; D016356:Gene Products, tax; D011518:Proto-Oncogene Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D012333:RNA, Messenger; D051028:bcl-2-Associated X Protein; D051020:bcl-X Protein; D019014:fas Receptor