G-CSF Receptor Blockade Ameliorates Arthritic Pain and Disease
Ming-Chin Lee, James A McCubbin, Anne D Christensen, Daniel P Poole, Pradeep Rajasekhar, TinaMarie Lieu, Nigel W Bunnett, Sonia Garcia-Caraballo, Andelain Erickson, Stuart M Brierley, Reem Saleh, Adrian Achuthan, Andrew J Fleetwood, Robin L Anderson, John A Hamilton, Andrew D Cook
JOURNAL OF IMMUNOLOGY | AMER ASSOC IMMUNOLOGISTS | Published : 2017
G-CSF or CSF-3, originally defined as a regulator of granulocyte lineage development via its cell surface receptor (G-CSFR), can play a role in inflammation, and hence in many pathologies, due to its effects on mature lineage populations. Given this, and because pain is an extremely important arthritis symptom, the efficacy of an anti-G-CSFR mAb for arthritic pain and disease was compared with that of a neutrophil-depleting mAb, anti-Ly6G, in both adaptive and innate immune-mediated murine models. Pain and disease were ameliorated in Ag-induced arthritis, zymosan-induced arthritis, and methylated BSA/IL-1 arthritis by both prophylactic and therapeutic anti-G-CSFR mAb treatment, whereas only ..View full abstract
Awarded by National Health and Medical Research Council of Australia
This work was supported by a grant from CSL Limited, a senior principal research fellowship (to J.A.H.), an R.D. Wright biomedical research fellowship (to S.M.B.) from the National Health and Medical Research Council of Australia, and by a postdoctoral fellowship from Novo Nordisk A/S, Denmark (to A.D. Christensen). J.A.H. and R.L.A. were supported by National Health and Medical Research Council of Australia Project Grant 1080560. D.P.P. and S.M.B. were supported by National Health and Medical Research Council of Australia Project Grant 1083480.