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Experimental arthritis

Stopping neutrophil migration in its tracks

Nature Reviews Rheumatology volume 13, page 3 (2017)Cite this article

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G-CSF, an important growth factor for neutrophil homeostasis and function, binds exclusively to G-CSFR, making it a promising therapeutic target for neutrophil- driven inflammatory diseases. “Our previous studies showed that G-CSF and G-CSFR-deficient mice were protected from various models of RA, while a G-CSF-neutralising monoclonal antibody (mAb) could reduce established disease,” asserts Campbell. “Previously, there were no available mAbs that could block mouse G-CSFR and so the effect of G-CSFR blockade on established disease could not be evaluated,” he explains.

Treatment with the anti-G-CSFR mAb ... reduced the number of neutrophils in the inflamed joints of mice

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References

  1. Campbell, I. K. et al. Therapeutic targeting of the G-CSF receptor reduces neutrophil trafficking and joint inflammation in antibody-mediated inflammatory arthritis. J. Immunol. http://dx.doi.org/10.4049/jimmunol.1600121 (2016)

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  1. Joanna Collison
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Collison, J. Stopping neutrophil migration in its tracks. Nat Rev Rheumatol 13, 3 (2017). https://doi.org/10.1038/nrrheum.2016.195

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