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Gamma irradiation up-regulates expression of B cell differentiation molecule CD23 by NF-kappaB activation.

Gamma irradiation (gamma-IR) is reported to have diverse effects on immune cell apoptosis, survival and differentiation. In the present study, the immunomodulatory effect of a low dose gamma-IR (5~10 Gy) was investigated, focusing on the role of NF-kappaB in the induction of the B cell differentiation molecule, CD23/FceRII. In the human B cell line Ramos, gamma-IR not only induced CD23 expression, but also augmented the IL-4-induced surface CD23 levels. While gamma-IR did not cause STAT6 activation in these cells, it did induce both DNA binding and the transcriptional activity of NF-kappaB in the IkappaB degradation-dependent manner. It was subsequently found that different NF-kappaB regulating signals modulated the gamma-IR-or IL-4-induced CD23 expression. Inhibitors of NF-kappaB activation, such as PDTC and MG132, suppressed the gamma-IR-mediated CD23 expression. In contrast, Ras, which potentiates gamma-IR-induced NF-kappaB activity in these cells, further augmented the gamma-IR- or IL-4-induced CD23 levels, The induction of NF-kappaB activation and the subsequent up-regulation of CD23 expression by gamma-IR were also observed in monocytic cells. These results suggest that gamma-IR, at specific dosages, can modulate immune cell differentiation through the activation of NF-kappaB, and this potentially affects the immune inflammatory response that is mediated by cytokines.