Another fork in the road: Foxo3a regulates NF-kappaB activation.
Previous studies have implicated the transcription factor FoxO3a in apoptosis induction. Thus, it comes as a surprise in this issue of Immunity that lymphoproliferative disease in Foxo3a-deficient mice may be due to T cell hyperactivity instead of cell death defects. Lin and colleagues provide important new evidence that disease development is associated with NF-kappaB hyperactivation in T cells.
Molecular Development Section, Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA.
Helen
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Su
Nicolas
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Bidere
Michael
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Lenardo
D000818:Animals; D000071316:Forkhead Box Protein O3; D051858:Forkhead Transcription Factors; D008232:Lymphoproliferative Disorders / Q000209:etiology / Q000378:metabolism; D051379:Mice; D016328:NF-kappa B / Q000276:immunology / Q000378:metabolism*; D019869:Phosphatidylinositol 3-Kinases / Q000276:immunology / Q000378:metabolism; D013601:T-Lymphocytes / Q000378:metabolism; D014157:Transcription Factors / Q000172:deficiency / Q000276:immunology / Q000378:metabolism*
D000071316:Forkhead Box Protein O3; D051858:Forkhead Transcription Factors; C474033:FoxO3 protein, mouse; D016328:NF-kappa B; D014157:Transcription Factors; D019869:Phosphatidylinositol 3-Kinases