Author/Authors :
Kitamura، نويسنده , , Hidemitsu and Ohta، نويسنده , , Akio and Sekimoto، نويسنده , , Masashi and Sato، نويسنده , , Marimo and Iwakabe، نويسنده , , Kenji and Nakui، نويسنده , , Minoru and Yahata، نويسنده , , Takashi and Meng، نويسنده , , Hongxu and Koda، نويسنده , , Toshiaki and Nishimura، نويسنده , , Shin-ichiro and Kawano، نويسنده , , Tetsu and Taniguchi، نويسنده , , Masaru and Nishimura، نويسنده , , Takashi، نويسنده ,
Abstract :
α-Galactosylceramide (α-GalCer), a glycolipid antigen, specifically activates natural killer T (NKT) cells by a CD1d-restricted mechanism. In this work, we found that in vivo administration of α-GalCer resulted in the activation of B cells in addition to NKT cells, namely, α-GalCer administration caused upregulation of the early activation marker, CD69, on both NKT and B cells. In addition, expression of B7.2 and I-Ab on B cells was greatly upregulated by α-GalCer. However, serum levels of IgE, IgG1, and IgG2a were not significantly changed within 48 h. In the present experiments, it was also demonstrated that the upregulation of CD69 expression by α-GalCer was strongly blocked by anti-IL-4 monoclonal antibody. Moreover, B-cell activation by α-GalCer was not observed in NKT-deficient mice. These results suggested that antigen-stimulated NKT cells might play a critical role not only in early defense mechanisms but also in early B-cell activation through IL-4 production.
Keywords :
?-galactocylceramide , B cell , CD69 , B7-2 , natural killer T cell