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

Abstract

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