Deciphering the Role of MOSPD2 in Rheumatoid Arthritis: Insights and Therapeutic Potential

Rheumatoid arthritis (RA) is a persistent inflammatory condition that impacts joints and is driven by B and T lymphocytes, which produce antibodies and pro-inflammatory cytokines. Innate immune cells, particularly monocytes, also contribute to the disease's progression by causing tissue damage. Genetic and pharmacological interventions targeting chemokine receptors CCR2 and CCR5 have been shown to reduce RA severity in preclinical models. MOSPD2, a 518-amino acid membrane protein, is expressed in monocytes and neutrophils and has been found to regulate their migration.

The study aimed to evaluate the role of MOSPD2 in monocyte migration and RA progression using anti-MOSPD2 monoclonal antibodies (mAbs). In vitro assays with MCP-1 and SDF-1 chemokines induced mouse splenic monocyte migration, which was inhibited by anti-MOSPD2 mAbs. In vivo, DBA-1 mice were subjected to arthritis induction with type II collagen, followed by treatment with anti-MOSPD2 mAb, anti-TNF-α, or isotype control antibody. The treatment with anti-MOSPD2 mAb was initiated after the onset of disease and showed significant inhibition of disease progression and clinical symptoms, reducing pannus formation and joint inflammation.

The findings underscore the importance of monocytes in RA and the potential therapeutic role of MOSPD2 in treating RA and other chronic inflammatory conditions.