Neutrophils persist in the joints of individuals with inflammatory arthritis, where they contribute to disease. The molecular basis of this persistence is now shown to hinge on the forkhead transcription factor Foxo3a. Foxo3a suppresses expression of Fas ligand, preventing neutrophil apoptosis (pages 666–671).
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References
Jonsson, H. et al. Nat. Med. 11, 666–671 (2005).
Tak, P.P. & Bresnihan, B. Arthritis Rheum. 43, 2619–2633 (2000).
Kremer, J.M. et al. N. Engl. J. Med. 349, 1907–1915 (2003).
Edwards, J.C. et al. N. Engl. J. Med. 350, 2572–2581 (2004).
Birkenkamp, K.U. & Coffer, P.J. J. Immunol. 171, 1623–1629 (2003).
Lin, L., Hron, J.D. & Peng, S. Immunity 21, 203–213 (2004).
Matsumoto, I. et al. Nat. Immunol. 3, 360–365 (2002).
Li, P. et al. Mol. Cell. Biol 23, 104–118 (2003).
Edwards, S.W. et al. Biochem. Soc. Trans. 32, 489–492 (2004).
Schubert, D. et al. Nat. Immunol. 3, 411 (2002).
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Liew, F., McInnes, I. A fork in the pathway to inflammation and arthritis. Nat Med 11, 601–602 (2005). https://doi.org/10.1038/nm0605-601
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DOI: https://doi.org/10.1038/nm0605-601
