G-CSF and GM-CSF as therapeutic targets in rheumatoid arthritis

Cornish, Ann L.
Campbell, Ian K.
McKenzie, Brent S.
Chatfield, Simon
Wicks, Ian P.

Autoimmunity and Transplantation Division, Walter and Eliza Hall Institute of Medical Research, Parkville, Vic, Australia (A. L. Cornish, S. Chatfield, I. P. Wicks). CSL, Bio21 Institute, Parkville, Vic, Australia (I. K. Campbell, B. S. McKenzie).

Correspondence: I. P. Wicks, Autoimmunity and Transplantation Division, Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade, Parkville, Vic 3052, Australia [email protected]

Competing interests

I. K. Campbell declares associations with the following companies: CSL, MorphoSys AG. B. S. McKenzie and I. P. Wicks declare associations with the following company: CSL. See the article online for full details of the relationships. The other authors declare no competing interests.

Nature Reviews Rheumatology 5(10):p 554-559, October 2009.

Abstract

Granulocyte colony-stimulating factor (G-CSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF) are well-recognized regulators of hematopoiesis and have an established role as growth factors in clinical practice. G-CSF and GM-CSF regulate myeloid cell production, differentiation and activation, and might also be important for driving inflammatory responses. Inappropriate engagement of this pathway could be a critical amplification mechanism when maladaptive immune responses predispose to autoimmunity and sterile tissue inflammation. We postulate that antagonism of G-CSF or GM-CSF could represent a novel therapeutic approach for a variety of autoimmune-mediated inflammatory diseases, including rheumatoid arthritis.

Cornish, A. L. et al. Nat. Rev. Rheumatol.5, 554-559 (2009); doi:10.1038/nrrheum.2009.178