AB0074 Interleukin-23 in Serum of Patients with Antineutrophil Cytoplasmic Antibody- Associated Systemic Vasculitis. (9th June 2015)

• Record Type: Journal Article
• Authors: Beketova, T.V.; Aleksandrova, E.N.; Nikonorova, N.O.; Nasonov, E.L.
• Is Part Of: Annals of the rheumatic diseases. Volume 74(2015)Supplement 2
• Page Start: 915
• Page End: 915
• Publication Date: 2015-06-09
• Subjects: Rheumatism -- Periodicals; 616.723005
• DOI: 10.1136/annrheumdis-2015-eular.2485
• Languages: English
• ISSNs: 0003-4967

Abstract

Abstract : Background: There is probably a systemic shift of cytokine production in patients with antineutrophil cytoplasmic antibody (ANCA)- associated systemic vasculitis (AAV) toward the Th17 cytokine response. We investigated whether interleukin-23 (IL-23), Th17- related cytokine, have any correlations with disease activity, clinical manifestations and treatment in AAV. Objectives: To analyse the concentration of interleukin-23 (IL-23) in serum of AAV patients, compared with healthy controls (HC). Methods: An enzyme- linked immunosorbent assay (ELISA) was used to analyse the serum concentration of IL-23 in 40 patients with AAV (median age 44 yrs (20- 65); F:M=1, 11) and 8 HC (median age 47 yrs (21- 66); F:M=1, 67). 23 patients were classified as granulomatosis with polyangiitis (GPA), 14- microscopic polyangiitis (MPA), and 3- eosinophilic granulomatosis with polyangiitis (EGPA). 26 patients were examined in active phase, 28- in remission (in 22/28 remission was induced by rituximab). The correlations between the levels of IL-23 and disease activity, clinical parameters were analysed. Results: The levels of IL-23 increased significantly in the serum of active PR3-ANCA patients before treatment compared with HC (median 41.9 pg/ ml and 13.1 pg/ ml, respectively, p<0, 05). As immunosuppressive and anti B cell therapy (rituximab) in AAV patients resulted in effective suppression of serum IL-23 (5, 2- 8, 8 pg/ ml). Conclusions: There is a prospect further study of IL-23 and functionally similar cytokines in the pathogenesis of AAV. Disclosure of Interest: None declared