Deletion of BST-1(CD157) Gene Impaired Systemic TI-2 Antigen-induced IgG3 and Mucosal TD Antigen-elicited IgA Responses

Motoyuki Itoh, Katsuhiko Ishihara,　Takachika Hiroi,� Byung Ok Lee, Hisoka Maeda, Hideki Iijima,� Manabu Yanagita,� Hiroshi Kiyono,� and Toshio Hirano.

Abstract

BST-1(CD157) deficient mice were generated in order to examine the immunological roles of the molecule in vivo. In BST-1-/- mice, the development of peritoneal B-1 cells were delayed and CD38low/- B lineage cells were increased in the bone marrow and spleen. Partial impairment of TI-2 and TD specific immune responses was noted in the systemic and mucosal compartments of BST-1 -/- mice, respectively. Although serum immunoglobulin levels as well as TD and TI-1 antigen-specific systemic immune responses were normal, TI-2 antigen-induced IgG3 response was selectively impaired. Oral immunization of BST-1-/- mice with cholera toxin, a potent TD antigen for the induction of IgA response, resulted in the poor production of antigen-specific antibodies at the intestinal mucosa accompanied by the reduced number of antigen-specific IgA producing cells in the lamina propria. These results indicate that BST-1 has roles in B cell development and antibody production in vivo.