Screening of the FDA-approved drug library identifies CCL17 inhibitors that block arthritic pain.

ABSTRACT: Rheumatoid arthritis (RA) is an inflammatory and destructive autoimmune polyarthritis that causes pain, swelling and deformity in the joints. While clinical trials targeting GM-CSF in RA are showing promise, the potential side effects of anti-GM-CSF therapy highlight the need for identifying downstream mediators of GM-CSF action. CCL17, a downstream inflammatory mediator of GM-CSF in monocytes and macrophages, has been shown to mediate GM-CSF-driven inflammatory arthritis in animal models. CCL17 shares its receptor, CCR4, with CCL22; however, unlike CCL17, CCL22 has been implicated in resolving inflammation. Therefore, drugs that can suppress the formation of CCL17, but not CCL22, may be beneficial in the treatment of inflammatory arthritis. In this study, we screened a panel of 1508 FDA-a

SUBMITTER: Eivazitork M 

PROVIDER: S-EPMC12287273 | biostudies-literature | 2025 Jul

REPOSITORIES: biostudies-literature