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Departments of
*
Pediatrics,
Blood Transfusion,
Parasitology, and
§
Obstetrics and Gynecology, Shinshu University School of Medicine, Matsumoto, Japan;
¶
Nagano Children’s Hospital, Toyoshina, Japan; and
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Department of Laboratory Sciences, School of Health Sciences, Faculty of Medicine, Kanazawa University, Kanazawa, Japan
The induction of IgE switching in B cells requires several signals
given by cytokines and cell contact-delivered signals. Here, we
investigated the role of CD27/CD70 interaction in B cell IgE synthesis.
The addition of CD27 ligand (CD70) transfectants to B cell cultures
increased the IgE synthesis synergistically in the presence of IL-4
plus anti-CD40 mAb (anti-CD40). The effect of CD70
transfectants was dose dependent and was completely blocked by
anti-CD70 mAb. CD27+ B cells had the ability to produce
IgE, which was increased by contact with CD70 transfectants, whereas
CD27- B cells did not produce IgE. CD27/CD70 interaction
enhanced B cell proliferation in the presence of IL-4 or IL-4 plus
anti-CD40. The augmentation of B cell proliferation by CD70
transfectants was apparent in CD27+ B cells, but was mild
in CD27- B cells. The helper activity for IgE synthesis by
the CD27/CD70 interaction did not contribute to the enhancement
of germline 
transcripts. Flow cytometric and morphological analyses
demonstrated that the addition of CD70 transfectants to B cell cultures
remarkably promoted differentiation into plasma cells in the presence
of IL-4 and CD40 signaling. Finally, CD27 cross-linking resulted in the
up-regulation of positive regulatory domain I-binding factor-1. Taken
together, our findings indicate that signaling via CD27 on B cells
induces IgE synthesis, in cooperation with IL-4 and CD40 signaling, by
promoting the generation of plasma cells through up-regulation of
positive regulatory domain I-binding factor-1.
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