Critical role for granulocyte colony stimulating factor in inflammatory arthritis

Kate E. Lawlor, Ian K. Campbell, Donald Metcalf, Kristy O'Donnell, Annemarie Van Nieuwenhuijze, Andrew W. Roberts, Ian P. Wicks

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91 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)11398-11403
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Issue number31
Publication statusPublished - 3 Aug 2004
Externally publishedYes

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