W204 - Elevated Levels of IL-35 in Different Stages of Rheumatoid Arthritis and Its Association with the Presence of Autoantibodies

Julio Castañeda-Delgado, PhD – Researcher for Mexico, National Council of Science and Technology (CONACYT-Mexico) Biomedical Research Unit of Zacatecas, Mexican Social Security Institute, Zacatecas, Mexico.; Irma González-Curiel, PhD – Academic Unit of Chemical Sciences, Autonomous University of Zacatecas, Jardín Juarez 147, Town 98000, Mexico.; Argelia López-Luna, PhD – Autonomous University of Zacatecas, Zacatecas, Mexico.; Christian Jacome-Galarza, PhD – Brigham and Whomen´s Hospital, Department of Medicine, Division of Rheumatology, Inflammation and Immunity, Harvard Medical School, Boston, MA; Bruno Rivas-Santiago, PhD – Zacatecas Biomedical Research Unit, Mexican Social Security Institute, Zacatecas, Mexico.; martin Zapata-Zuñiga, PhD – Rural Hospital No 51, Mexican Social Security Institute, Villanueva, Zacatecas, Mexico; Faculty of Medicine and Health Sciences, Autonomous University of Zacatecas, Zacatecas, Mexico.

Abstract Text: Rheumatoid arthritis can cause pain, inflammation and destruction of joints. IL-35 is a recently described immunosuppressive and anti-inflammatory cytokine. Several roles of IL-35 in the immune and inflammatory regulation of autoimmune diseases have been described. In this work we determined the relationship among the serum concentrations of IL-35 expressed in different stages of RA pathology and its association with autoantibodies. Donor samples were collected (n=64): 1) Healthy, 2) CCP+, 3) Patients with early Arthritis, 4) Patients with established rheumatoid arthritis according to ACR-AULAR classification. Determinations of IL-35 were made by ELISA according to manufacturer´s instructions. Statistical analysis was carried out in Graph Pad Prism software. No significant differences were identified on the proportions of clinical variables and demographics among groups. A statistically significant difference (P < 0.05) was identified when analyzing the concentrations of IL-35 in the CCP+ group compared to controls. This was more pronounced than those on early and established RA. Additionally associations with autoantibodies were identified for both CCP and CarP autoantibodies and other clinically relevant variables. Our data suggest an important clinically relevant link among IL-35 and the presence of autoantibodies, particularly CCP. The clinical implications of such results await further experimentation.