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The Pre-B Cell Receptor Signaling for Apoptosis Is Negatively Regulated by FcRIIB¹

Ibuki Kato^*, Toshiyuki Takai and Akira Kudo^*

^* Department of Life Science, Tokyo Institute of Technology, Yokohama, Japan; Institute of Development, Aging and Cancer, Tohoku University, Sendai, Japan

Many studies have shown that FcRIIB is a negative regulator of B cell receptor signaling, and even though FcRIIB is expressed through all developmental stages of the B cell lineage, its involvement in pre-B cell receptor (pre-BCR) signaling has not been examined. To investigate FcRIIB function at the pre-B cell stage, we have established pre-BCR positive pre-B cell lines from normal mice and FcRIIB-deficient mice, named PreBR and Fc^-/-PreBR, respectively. These cell lines are able to differentiate into immature B cells in vitro by removal of IL-7. In PreBR, apoptosis was moderately induced by F(ab')₂ anti-µ Ab, but not by intact anti-µ Ab. Phosphorylation of SH2-containing inositol 5-phosphatase (SHIP) and Dok, which are involved in FcRIIB signaling, was induced by anti-µ cross-linking in PreBR. In contrast, apoptosis was strongly induced by both the F(ab')₂ and intact anti-µ Abs in Fc^-/-PreBR, and the level of phosphorylation of SHIP or Dok was much lower in Fc^-/-PreBR than those observed in PreBR. Restoration of FcRIIB to Fc^-/-PreBR followed by anti-µ cross-linking blocked severe apoptosis, and up-regulated SHIP and Dok phosphorylation. The results demonstrate that FcRIIB negatively regulates pre-BCR-mediated signaling for apoptosis.

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