Activation of Transcription Factors in Inflammatory Diseases

Louis, MO, USA) worked with a line of mice with immune deficiencies that mimicked the human autoimmune disease lupus. They reported in the February 13, 2004, issue of Science that in these animals Foxj1 activity was depressed, and the lack of the Foxj1 protein product increased the activity of another transcription factor, NF-B (nuclear factor-B). Many of the genes that are responsive to NF-B play key roles in the regulation of inflammatory and immune responses. Deregulation of NF-B activity is often observed in several chronic and acute inflammatory diseases.

"We used to think of mature immune cells like T cells and B cells as metabolically inactive when waiting for infections or other signals that trigger an attack,” explained senior author Dr. Stanford Peng, assistant professor of internal medicine, pathology, and immunology at Washington University School of Medicine. "We are now thinking these resting cells actually are very metabolically active, and they are kept in a quiescent state by genes actively working to shut down activating proteins.”




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