Interleukin-29 and interleukin-28A induce migration of neutrophils in rheumatoid arthritis.

Abstract

Type III Interferons, interleukin (IL)-29 and IL-28A, have been implicated in the inflammatory response of rheumatoid arthritis (RA). Increasing evidence suggests an important role of neutrophils in the pathogenesis of RA. However, the underlying mechanism remains unclear. Therefore, we investigated the expression of the receptor of these type III interferons, IL-28R1, on the neutrophils of RA patients, and further explored the roles of IL-29 and IL-28A on neutrophil activity. Neutrophils were extracted from peripheral blood of patients who met the diagnostic criteria for RA and healthy controls. The serum levels of IL-29 and IL-28A in RA patients and healthy controls were examined by enzyme-linked immunoassay, and the expression of IL-28R1 on neutrophils was determined by flow cytometry. A transwell assay was performed to determine the chemotactic ability of IL-29 and IL-28A to neutrophils in RA patients. The serum IL-29 but not IL-28A levels were significantly elevated in RA patients, and neither was correlated with RA disease activity. IL-28R1 levels on neutrophils were significantly (p < 0.001) elevated in patients with RA (51.85% (36.10%, 67.03%)) compared with those of healthy controls (4.13% (3.54%, 7.96%)), and IL-29 and IL-28A had a significant chemotactic effect on neutrophils from the peripheral blood of RA patients. IL-29 and IL-28A play an important role in regulating neutrophils which participate in the pathogenesis of RA. Therefore, inhibiting IL-29 and IL-28A may be a new therapeutic strategy for RA. Key points • The IL-28R1 levels were increased in neutrophils of RA patients, suggesting its potentially important role in the pathogenesis of RA. • IL-29 and IL-28A induce the migration of neutrophils that participate in the development of RA.