[摘要]：We previously reported that I kappa BL prevents experimental autoimmune arthritis. The molecular mechanism, however, still remains unclear. In contrast to four splicing-isoforms of I kappa BL in human, two isoforms were identified in mouse. The major isoform I kappa BL-alpha(S) suppressed LPS-induced NF-kappa B activation and transcription of TNF alpha and IL-6, but not IL-1 beta. The suppressive activity required the nuclear localization signal and the ankyrin repeat domain of I kappa BL. I kappa BL did not affect the nuclear translocation of the NF-kappa B dimer. These findings point to I kappa BL as being a novel member of the nuclear I kappa B family, which functions in the nucleus and controls various inflammatory responses including autoimmune arthritis. (C) 2011 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
