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Coordination of NF-B and NFAT Antagonism by the Forkhead Transcription Factor Foxd1¹

Ling Lin^* and Stanford L. Peng^2,*,

^* Division of Rheumatology, Department of Internal Medicine, and Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110

Forkhead transcription factors play critical roles in the maintenance of immune homeostasis. In this study, we demonstrate that this regulation most likely involves intricate interactions between the forkhead family members and inflammatory transcription factors: the forkhead member Foxd1 coordinates the regulation of the activity of two key inflammatory transcription factors, NF-AT and NF-B, with Foxd1 deficiency resulting in multiorgan, systemic inflammation, exaggerated Th cell-derived cytokine production, and T cell proliferation in autologous MLRs. Foxd1-deficient T cells possess increased activity of both NF-AT and NF-B: the former correlates with the ability of Foxd1 to regulate casein kinase 1, an NF-AT inhibitory kinase; the latter with the ability of Foxd1 to regulate Foxj1, which regulates the NF-B inhibitory subunit IB. Thus, Foxd1 modulates inflammatory reactions and prevents autoimmunity by directly regulating anti-inflammatory regulators of the NF-AT pathway, and by coordinating the suppression of the NF-B pathway via Foxj1. These findings indicate the presence of a general network of forkhead proteins that enforce T cell quiescence.

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