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Members of the NF-κB/RelB family of transcription factors play important roles in the regulation of inflammatory and immune responses. RelB, a member of this family, has been characterized as a transcription activator and is involved in the constitutive NF-κB activity in lymphoid tissues. However, in a previous study we observed an overexpression of chemokines in RelB-deficient fibroblasts. Here we show that RelB is an important transcription suppressor in fibroblasts which limits the expression of proinflammatory mediators and may exert its function by modulating the stability of IκBα protein. Fibroblasts fromrelb −/− mice overexpress interleukin-1α (IL-1α), IL-1β, and tumor necrosis factor alpha in response to lipopolysaccharide (LPS) stimulation. These cells have an augmented and prolonged LPS-inducible IKK activity and an accelerated degradation which results in a diminished level of IκBα protein, despite an upregulated IκBα mRNA expression. Consequently, NF-κB activity was augmented and postinduction repression of NF-κB activity was impaired in these cells. The increased κB-binding activity and cytokine overexpression was suppressed by introducing RelB cDNA or a dominant negative IκBα intorelb −/− fibroblasts. Our findings suggest a novel transcription suppression function of RelB in fibroblasts.

molecular and cellular biology

RelB Modulation of IκBα Stability as a Mechanism of Transcription Suppression of Interleukin-1α (IL-1α), IL-1β, and Tumor Necrosis Factor Alpha in Fibroblasts