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Immunol Lett. 2017 Oct;190:177-184. doi: 10.1016/j.imlet.2017.08.008. Epub 2017 Aug 12.

Interleukin-26 is overexpressed in Behçet's disease and enhances Th17 related -cytokines.

Author information

1
Unit Research 12SP15 "Expression moléculaire des interactions cellulaires et leur mode de communication dans le poumon profond", A. Mami Hospital, Ariana, Tunisia; Université de Tunis El Manar, Faculty of Medicine of Tunis, Department of Basic Sciences, Tunis, Tunisia.
2
Unit Research 12SP15 "Expression moléculaire des interactions cellulaires et leur mode de communication dans le poumon profond", A. Mami Hospital, Ariana, Tunisia; Université de Tunis El Manar, Faculty of Medicine of Tunis, Department of Basic Sciences, Tunis, Tunisia; Division of Pulmonology, Department of Paediatric Respiratory Diseases, Abderrahman Mami Hospital, Pavillon B, Ariana, Tunisia.
3
Unit Research 12SP15 "Expression moléculaire des interactions cellulaires et leur mode de communication dans le poumon profond", A. Mami Hospital, Ariana, Tunisia; Laboratory of Clinical Virology, Pasteur Institute, Tunis, Tunisia.
4
Unit Research 12SP15 "Expression moléculaire des interactions cellulaires et leur mode de communication dans le poumon profond", A. Mami Hospital, Ariana, Tunisia; Université de Tunis El Manar, Faculty of Medicine of Tunis, Department of Basic Sciences, Tunis, Tunisia. Electronic address: Kamel.hamzaoui@gmail.com.

Abstract

Behçet's disease (BD) is a multi-systemic inflammatory disorder characterized by the "triple symptom complex". Several pro-inflammatory cytokines, mainly derived from the immune Th17 axis, seem to be involved in different pathogenic pathways leading to development of the clinical manifestations. Here, we have analyzed the expression and role of IL-26 in active BD patients, an inflammatory disorder characterized by bronchoalveolar lavage fluid (BAL) and cerebrospinal fluid (CSF) inflammation. On this basis, the primary aim of our work was to study IL-26 levels in serum, BAL CSF) from active BD patients. Samples were collected from 95 BD patients (55 patients were in active stage) and 50 healthy controls (HC). They were investigated with ELISA for estimation of cytokines levels. Serum concentration of IL-26 resulted higher in both active [4.80±1.32] and inactive [2.77±1.026] BD than HC [0.31±0.14ng/ml; p<0.0001]. Level of IL-26 was associated with the BD clinical severity score from moderate to severe (P<0.0001). IL-26 was highly expressed in CSF [10.80±2.05ng/ml] and in BAL [12.89±3.03ng/ml] fluid from BD patients comparatively to their respective controls. IL-26 levels in CSF and in BAL fluid showed positive correlations with IL-17 level and an inversely correlation with IL-37. Interestingly, IL-26-stimulated CD4+ T cells and monocytes promote the generation of Th17 (IL-17A, IL-23) and suppress Treg (IL-10, TGF-β) cytokines. Our findings may suggest a signature of IL-26 probably responsible for the inflammatory process to correlate positively with Th17 cytokines and inversely with Treg mediators. This evidence could contribute to improve the knowledge regarding the role of IL-26 in BD severity. For the first time, IL-26 expression is demonstrated in BAL and CSF, supporting a role for this cytokine in the pathogenesis of BD. IL-26 thereby appears as a novel proinflammatory cytokine favoring the generation of Th17 cytokines.

KEYWORDS:

Behcet disease severity; Bronchoalveolar lavage; Cerebrospinal fluid; IL-26; Inflammation; Th17; Treg

PMID:
28811236
DOI:
10.1016/j.imlet.2017.08.008
[Indexed for MEDLINE]

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