Treatment for rheumatoid arthritis by chemokine blockade.
Chemokines induce migration of inflammatory cells. In the synovial tissue of rheumatoid arthritis (RA), abundant chemokines are expressed, which contribute migration of lymphocytes and monocytes/macrophages, stimulation of synovial cells, and angiogenesis. Blockade of CCL2, CCL3, CCL5, CCR1, CCR9, CXCL2, CXCL5, CXCL13, CXCL16, CXCR3, CXCR4, CXCR7, and CX3CL1 showed improvement of arthritis of animal models. Moreover, CCR1 antagonist and anti-CXCL10 antibody reduced arthritis of patients with RA. Chemokine is a promising target for RA therapy.
Division of Rheumatology, Department of Internal Medicine, Toho University School of Medicine.
Toshihiro
T
Nanki
D000818:Animals; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D001172:Arthritis, Rheumatoid / Q000188:drug therapy* / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D002465:Cell Movement; D054357:Chemokine CXCL10 / Q000276:immunology; D018925:Chemokines / Q000037:antagonists & inhibitors* / Q000378:metabolism; D004195:Disease Models, Animal; D006801:Humans; D018836:Inflammation Mediators / Q000037:antagonists & inhibitors* / Q000378:metabolism; D008214:Lymphocytes / Q000473:pathology; D008264:Macrophages / Q000473:pathology; D058990:Molecular Targeted Therapy; D009000:Monocytes / Q000473:pathology; D009389:Neovascularization, Pathologic; D054389:Receptors, CCR1 / Q000037:antagonists & inhibitors; D019707:Receptors, Chemokine / Q000627:therapeutic use*; D013583:Synovial Membrane / Q000098:blood supply / Q000166:cytology / Q000378:metabolism
D000911:Antibodies, Monoclonal; C515300:CCR1 protein, human; D054357:Chemokine CXCL10; D018925:Chemokines; D018836:Inflammation Mediators; D054389:Receptors, CCR1; D019707:Receptors, Chemokine