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).
This is a preview of subscription content, log in via an institution to check access.
Katie Ris
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).
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
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
Issue Date:
DOI: https://doi.org/10.1038/nm0605-601
- Springer Nature America, Inc.