title: Human leukocyte antigen-class II-negative long-term cultured human T-cell leukemia virus type-I-infected T-cell lines with progressed cytological properties significantly induce superantigen-dependent normal T-cell proliferation.
abstract: While most human T-cell leukemia virus type-I (HTLV-I)-infected T cells express abundant class II antigens, some aggressive-type adult T-cell leukemia (ATL) cells lose their expression. To investigate the significance of the class II antigen of HTLV-I infected cells, the progressiveness of HTLV-I-infected long-term cultured T-cell lines was evaluated, and then their antigen-presenting capacity was examined using a superantigen, staphylococcus enterotoxin B (SEB). Among the cell lines derived from peripheral blood, HPB-ATL-T (ATL-T), HPB-ATL-2 (ATL-2) and HPB-ATL-O were more progressed than Tax exclusively expressing HPB-CTL-I (CTL-I), because the former deleted p16 gene (polymerase chain reaction (PCR)) and strongly transcribed survivin (reverse transcriptase-PCR). Notably, interferon gamma-independent loss of class II expression of ATL-T and ATL-2 was found. In antigen-presenting experiments, however, both cell lines induced SEB-dependent significant T-cell proliferation estimated by [(3)H] thymidine uptake. No class II-re-expressed ATL-2 cells were observed in the SEB-presenting cultures by indirect immunofluorescence, and only minimum inhibition of SEB-dependent T-cell response by anti-human leukocyte antigen (HLA)-DR monoclonal antibody was observed. These findings suggest that both ATL-T and ATL-2 very effectively present SEB to T cells less dependently on class II molecules. These less immunogenic leukemic cells of aggressive ATL may contribute to disease aggression.
authors.affiliation: Clinical Laboratory, Hamada Medical Center, Shimane, Japan. mnagasaki@hamamda2.hosp.gp.jp
authors.forename: Makoto
authors.initials: M
authors.lastname: Nagasaki
authors.forename: Jie
authors.initials: J
authors.lastname: Zhang
authors.forename: Shigeru
authors.initials: S
authors.lastname: Morikawa
authors.forename: Takayuki
authors.initials: T
authors.lastname: Harada
authors.forename: Toru
authors.initials: T
authors.lastname: Nabika
authors.forename: Yuetsu
authors.initials: Y
authors.lastname: Tanaka
mesh_terms: D000328:Adult; D017951:Antigen Presentation; D000942:Antigens, Bacterial / Q000276:immunology / Q000502:physiology; D002460:Cell Line; D049109:Cell Proliferation; D004768:Enterotoxins / Q000276:immunology / Q000502:physiology; D005434:Flow Cytometry; D015870:Gene Expression / Q000187:drug effects; D006684:HLA-DR Antigens / Q000235:genetics* / Q000276:immunology; D015486:HTLV-I Antigens / Q000276:immunology / Q000502:physiology; D015368:Human T-lymphotropic virus 1 / Q000254:growth & development*; D006801:Humans; D051034:Inhibitor of Apoptosis Proteins; D007371:Interferon-gamma / Q000378:metabolism / Q000494:pharmacology; D015458:Leukemia, T-Cell / Q000235:genetics / Q000276:immunology; D008869:Microtubule-Associated Proteins / Q000235:genetics; D009363:Neoplasm Proteins; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D018089:Superantigens / Q000276:immunology / Q000502:physiology*; D000077022:Survivin; D013601:T-Lymphocytes / Q000166:cytology / Q000276:immunology* / Q000821:virology; D014158:Transcription, Genetic
chemical_list: D000942:Antigens, Bacterial; C107489:BIRC5 protein, human; D004768:Enterotoxins; D006684:HLA-DR Antigens; D015486:HTLV-I Antigens; D051034:Inhibitor of Apoptosis Proteins; D008869:Microtubule-Associated Proteins; D009363:Neoplasm Proteins; D012333:RNA, Messenger; D018089:Superantigens; D000077022:Survivin; C031818:enterotoxin B, staphylococcal; D007371:Interferon-gamma