Author/Authors :
Watanabe، نويسنده , , Tomoko and Masuyama، نويسنده , , Jun-ichi and Sohma، نويسنده , , Yoshiaki and Inazawa، نويسنده , , Hiroko and Horie، نويسنده , , Kaori and Kojima، نويسنده , , Kumiko and Uemura، نويسنده , , Yasunori and Aoki، نويسنده , , Yumi and Kaga، نويسنده , , Shuji and Minota، نويسنده , , Seiji and Tanaka، نويسنده , , Toshiyuki and Yamaguchi، نويسنده , , Yasunori and Kobayashi، نويسنده , , Tetsuto ، نويسنده ,
Abstract :
We previously reported that 4C8 monoclonal antibody (mAb) provides a costimulatory signal to human CD4+ T cells and consequently induces regulatory T (Treg) cells, which are hypo-responsive and suppress the polyclonal response of bystander CD4+ cells in a contact-dependent manner. In this study, we identified the antigen of 4C8 mAb as CD52. Costimulation with Campath-1H, a humanized anti-CD52 mAb, also induced Treg cells. Anti-CD52-induced Treg cells suppressed the proliferation of both CD4+ and CD8+ T cells provided with polyclonal or allogeneic stimulation. When Treg cells were induced from Staphylococcal enterotoxin B (SEB) treated cells, they suppressed the response to SEB more efficiently than that to another superantigen, SEA. Furthermore, anti-CD52-induced Treg cells could be expanded by culture with IL-2 followed by CD52-costimulation, and co-injection of expanded Treg cells suppressed lethal xenogeneic graft versus host disease (GvHD) reactions in SCID mice caused by human peripheral blood mononuclear cells (PBMCs).
Keywords :
T cells , Regulatory T cells , Suppressor T cells , human
