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-${kappa}B$ 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-${kappa}B$ in the $I{kappa}B$ degradation-dependent manner. It was subsequently found that different NF-${kappa}B$ regulating signals modulated the $gamma$-IR-or IL-4-induced CD23 expression. Inhibitors of NF-${kappa}B$ activation, such as PDTC and MG132, suppressed the $gamma$-IR-mediated CD23 expression. In contrast, Ras, which potentiates $gamma$-IR-induced NF-${kappa}B$ activity in these cells, further augmented the $gamma$-IR- or IL-4-induced CD23 levels, The induction of NF-${kappa}B$ 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-${kappa}B$, and this potentially affects the immune inflammatory response that is mediated by cytokines.