A monoclonal antibody against a murine CD38 homologue delivers a signal to B cells for prolongation of survival and protection against apoptosis in vitro: unresponsiveness of X-linked immunodeficient B cells.

分子生物学 生物 细胞凋亡 脾脏 CD38 程序性细胞死亡 单克隆抗体 B细胞 体外 布鲁顿酪氨酸激酶 抗体 细胞生物学 免疫学 干细胞 信号转导 生物化学 酪氨酸激酶 川地34
作者
Yoshio Yamashita,Kensuke Miyake,Y. Kikuchi,Kiyoshi Takatsu,Shinichi Noda,Akihiko Kosugi,Masao Kimoto
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期刊:PubMed 卷期号:85 (2): 248-55 被引量:42
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A novel monoclonal antibody (mAb) was established in an attempt to look for a cell-surface molecule that delivered a signal regulating apoptotic cell death of B cells. Because spleen cells in resting culture die from apoptosis, mAb were looked for that were able to prolong spleen cell survival in vitro. This screening selected mAb CS/2. CS/2 not only prolonged spleen cell survival in vitro, but also protected spleen cells from apoptotic cell death brought about by irradiation or dexamethasone. Moreover, stimulation of spleen cells with CS/2 mAb induced changes of cells to blastoid morphology, and a significant uptake of [3H]thymidine ([3H]TdR). The antigen recognized by CS/2 mAb (CS/2 Ag) was expressed on preB cells, B cells, and Mac-1+ cells. The cells surviving in vitro culture or irradiation in response to ligation with CS/2 mAb were mostly B cells expressing the CS/2 Ag. In addition, B cells from X-linked immunodeficient (XID) mice did not respond to CS/2 mAb. These results indicate that CS/2 mAb is agonistic to B cells, and that XID mice are deficient in this CS/2 mAb-mediated activation pathway. Determination of the amino-terminal 24 amino acid residues revealed that the CS/2 Ag appears to be identical to the CS/2 mAb is directed against a murine CD38 homologue, and suggest a possible role of the murine CD38 homologue in controlling apoptotic cell death of B cells.

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