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IL-17 and IL-23 in lupus nephritis - association to histopathology and response to treatment
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Clinical Immunology.ORCID iD: 0000-0003-1186-3226
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2015 (English)In: BMC Immunology, ISSN 1471-2172, E-ISSN 1471-2172, Vol. 16, article id 7Article in journal (Refereed) Published
Abstract [en]

Background: Recent studies indicate a central role for the IL-23/IL-17 axis in the pathogenesis of lupus nephritis (LN) but the importance in the context of treatment outcome is unknown. We studied various cytokines, including the IL-23/IL-17 axis, in association to histopathology and response to therapy. Methods: Fifty-two patients with active LN were included. Renal biopsies were performed at baseline and after immunosuppressive treatment. Serum levels of TNF-alpha, IFN-gamma, IL-6, IL-10, IL-17, IL-23 and TGF-beta were analysed at both biopsy occasions and in 13 healthy controls. IL-17 expression in renal tissue was assessed by immunohistochemistry. Biopsies were evaluated regarding WHO-classification and renal disease activity was estimated using the BILAG-index. Improvement of 2 grades in renal BILAG was regarded complete response, and 1 grade partial response. Results: At baseline, all patients had high disease activity (BILAG A/B). Baseline levels of IL-6, IL-10, IL-17, IL-23 (p < 0.001) and IFN-gamma (p = 0.03) were increased in patients vs. controls. In contrast, TGF-beta was lower in patients compared to controls (p < 0.001). Baseline levels of IL-17 were higher in patients with persisting active nephritis (WHO III, IV, V) after treatment, i.e. a poor histological response, vs. WHO I-II (p < 0.03). At follow-up, IL-23 were higher in BILAG-non-responders vs. responders (p < 0.05). Immunostaining of renal tissue revealed IL-17 expression in inflammatory infiltrates. Conclusions: High baseline IL-17 predicted an unfavourable histopathological response, and BILAG-non-responders had high IL-23, indicating that that a subset of LN-patients has a Th-17 phenotype that may influence response to treatment and could be evaluated as a biomarker for poor therapeutic response.

Place, publisher, year, edition, pages
2015. Vol. 16, article id 7
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Immunology in the medical area
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URN: urn:nbn:se:uu:diva-249015DOI: 10.1186/s12865-015-0070-7ISI: 000350621300002OAI: oai:DiVA.org:uu-249015DiVA, id: diva2:807818
Available from: 2015-04-24 Created: 2015-04-10 Last updated: 2018-02-27Bibliographically approved

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