Volume 19, Issue 10 pp. 1803-1809
Article
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Activation of human t cells by toxic shock syndrome toxin-1: the toxin-binding structures expressed on human lymphoid cells acting as accessory cells are hla class ii molecules

Takehiko Uchiyama

Corresponding Author

Takehiko Uchiyama

Department of Microbiology, Tokyo Women's Medical College

The Department of Microbiology Tokyo Women's Medical College, 8–1 Kawada-cho, Shinjuku-ku, Tokyo 162, JapanSearch for more papers by this author
Ken'Ichi Imanishi

Ken'Ichi Imanishi

Department of Microbiology, Tokyo Women's Medical College

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Shinji Saito

Shinji Saito

Department of Microbiology, Tokyo Women's Medical College

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Minako Araake

Minako Araake

Department of Microbiology, Tokyo Women's Medical College

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Xiao-Jie Yan

Xiao-Jie Yan

Department of Microbiology, Tokyo Women's Medical College

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Hiroshi Fujikawa

Hiroshi Fujikawa

Department of Microbiology, Tokyo Metropolitan Research Laboratories of Public Health, Tokyo

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Hideo Igarashi

Hideo Igarashi

Department of Microbiology, Tokyo Metropolitan Research Laboratories of Public Health, Tokyo

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Hidehito Kato

Hidehito Kato

Department of Transplantation Immunology, Kitasato University School of Medicine

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Fumiya Obata

Fumiya Obata

Department of Transplantation Immunology, Kitasato University School of Medicine

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Noboru Kashiwagi

Noboru Kashiwagi

Department of Transplantation Immunology, Kitasato University School of Medicine

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Hidetoshi Inoko

Hidetoshi Inoko

Department of Transplantation, Tokai University School of Medicine

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First published: October 1989
Citations: 34

Abstract

Toxic shock syndrome toxin-1 (TSST-1)-binding assay using 125I-labeled TSST-1 showed the presence of specific TSST-1 binding in a B cell fraction of human peripheral blood mononuclear cells and L cells transfected with DR2 genes or DR4 genes but not in a T cell fraction and control L cells. Fixation with paraformaldehyde, an inhibitor of antigen processing, did not remove TSST-1-binding activity of the transfectants. Binding of 125I-labeled TSST-1 to the transfectants was reduced by an anti-DR monoclonal antibody. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis revealed the presence of a single band with TSST-1-binding activity and the same migration pattern as DR heterodimers. TSST-1-induced T cell responses, proliferation and interleukin 2 (IL2) production were observed in the presence of the transfectants but not in the presence of control L cells, while concanavalin A-induced IL2 production was observed in the presence of either the transfectants or control L cells. Presence of an anti-DR monoclonal antibody inhibited the TSST-1-induced responses. Paraformaldehyde-fixed Daudi cells were effective in supporting TSST-1-induced IL2 production by T cells. These results indicate that HLA class II molecules directly bind intact TSST-1 and perform an essential role as the TSST-1-binding structures on accessory cells in T cell activation by the toxin.

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