Conclusion
Our findings suggest a pathogenic role of IGFBP6 in RA and support its possible targeting for therapeutic purposes.
Methods
IGFBP6 was measured in RA patients and healthy donors (HD) sera by Luminex xMAP® technology and in ST of RA patients and osteoarthritis (OA) controls by immunofluorescence. The identification of circulating IGFBP6+ cells was evaluated by flow cytometry and an in vitro migration assay was arranged.
Results
We demonstrated that IGFBP6 is able to induce greater in vitro migration of RA as compared to HD and OA T lymphocytes and is overexpressed in serum and ST of RA patients. This in vitro chemotactic activity can be partially inhibited by dexamethasone.