Critical role for granulocyte colony-stimulating factor in inflammatory arthritis
- Author(s)
- Lawlor, KE; Campbell, IK; Metcalf, D; O'Donnell, K; van Nieuwenhuijze, A; Roberts, AW; Wicks, IP;
- Details
- Publication Year 2004-08-03,Volume 101,Issue #31,Page 11398-11403
- Journal Title
- PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
- Publication Type
- Journal Article
- Abstract
- Granulocyte colony-stimulating factor (G-CSF) is a well known regulator of granulopoiesis, but the role of endogenous G-CSF in inflammatory joint disease has not been explored. We studied the response of G-CSF-deficient mice in experimental models of joint inflammation. We show that G-CSF deficiency protects mice from acute and chronic arthritis. Reduced severity was associated with blunted mobilization of granulocytic cells from the bone marrow and less cellular infiltrate and cellular activation in inflamed joints. We also demonstrate that G-CSF blockade in established collagen-induced arthritis in WT mice markedly reduces disease manifestations and is as effective as tumor necrosis factor blockade. Our results reveal a critical role for G-CSF in driving joint inflammation and highlight G-CSF as a potential therapeutic target in inflammatory joint diseases, such as rheumatoid arthritis.
- Publisher
- NATL ACAD SCIENCES
- Keywords
- FACTOR G-CSF; COLLAGEN-INDUCED ARTHRITIS; STEM-CELL MOBILIZATION; RHEUMATOID-ARTHRITIS; ENDOTHELIAL-CELLS; PERIPHERAL-BLOOD; NECROSIS-FACTOR; DEFICIENT MICE; IN-VIVO; T-CELLS
- Publisher's Version
- https://doi.org/10.1073/pnas.0404328101
- Terms of Use/Rights Notice
- Refer to copyright notice on published article.
Creation Date: 2004-08-03 12:00:00