Interferon-β inhibits inflammatory responses mediators via suppression of iNOS signaling pathway in PBMCs from patients with primary Sjögren’s syndrome

Benchabane, Sarah; Belkhelfa, Mourad; Belguendouz, Houda; Zidi, Sourour; Boudjelida, A.; Youinou, Pierre; Touil-Boukoffa, Chafia

doi:10.1007/s10787-018-0499-4

Cited by 8 publications

(4 citation statements)

References 40 publications

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“…However, the results of Benchabane's group suggested that IFN-β restored immune balance between inflammatory and anti-inflammatory responses by reducing pro-inflammatory cytokines in peripheral blood mononuclear cells from SS patients. Therefore, it seemed that IFN-β had beneficial impact in SS 47. Therefore, further studies are needed to uncover the exact role and precise mechanisms of IFN-β in SS.…”

Section: Discussionmentioning

confidence: 99%

Mesenchymal stem cell transplantation alleviates experimental Sjögren's syndrome through IFN-β/IL-27 signaling axis

Yao¹,

Qi²,

Liang³

et al. 2019

Theranostics

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Rationale: Although mesenchymal stem cell (MSC) transplantation has been proved to be an effective therapeutic approach to treat experimental Sjögren's syndrome (SS), the detailed underlying mechanisms remains unknown. IL-27 has diverse influences on the regulation of T cell differentiation and was involved in SS through modulating immune response. Here we aimed to explore whether IL-27-mediated regulation of immune cells was responsible for the beneficial effects of MSC transplantation on SS.Methods: The SS-like symptoms were evaluated in IL-27 deficient and recombinant IL-27-treated NOD mice. The MSCs were infused into NOD mice via the tail vein. The histological features of submandibular glands, saliva flow rate and serum IL-27 were examined. The effects of MSCs on the IL-27 production and Th17/Treg cell in SS patients and mice in vitro and in vivo were determined for the mechanistic study.Results: This study showed that SS patients had decreased IL-27 level and increased ratio of Th17/Treg cells. Consistently, exacerbated SS-like symptoms were observed in IL-27 deficient NOD mice, along with increased ratio of Th17/Treg cells. Importantly, MSC transplantation alleviated SS-like symptoms by elevating the level of IL-27 to restore Th17/Treg balance in NOD mice. Mechanistically, MSC-secreted interferon-β (IFN-β) promote dendritic cells to produce IL-27.Conclusions: Thus, we have revealed a previously unrecognized function of MSC-mediated IL-27 production by DCs in suppressing SS-like syndrome, which provided evidences for clinical application of MSC in patients with SS.

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Section: Discussionmentioning

confidence: 99%

Mesenchymal stem cell transplantation alleviates experimental Sjögren's syndrome through IFN-β/IL-27 signaling axis

Yao¹,

Qi²,

Liang³

et al. 2019

Theranostics

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“…In accordance, recent research findings highlight a consistent ex vivo inhibitory effect of IFN- β on proinflammatory cytokine production and NO pathway in pSS patients. These data suggest that IFN- β could represent a potential candidate for targeting inflammation during pSS [30].…”

Section: Discussionmentioning

confidence: 99%

Sjögren’s Syndrome: Concerted Triggering of Sicca Conditions

Mackiewicz

Mażul

Narkevičiūtė

et al. 2019

Journal of Immunology Research

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Aim The aim of this study was to evaluate the expression of persistence of mumps virus and some cells that interact with viral infection in the focus of the autoimmune epithelitis and peripheral blood of Sjögren's syndrome patients in comparison to patients with rheumatoid arthritis (RA) and nonautoimmune sicca syndrome (nSS). Materials and Methods 126 patients (119 women and 7 men) were grouped into four groups: (1) patients with primary Sjögren's syndrome (pSS), (2) patients with secondary Sjögren's syndrome due to rheumatoid arthritis (sSS), (3) patients with rheumatoid arthritis (RA), and (4) patients with nonautoimmune sicca syndrome (nSS). Immunohistochemical analysis of immune response to the suggested silent persistence of mumps virus in the minor labial salivary gland biopsies and flow cytometric analysis of blood cells was done. Results Immunohistochemical signs of mumps virus persistence were found in the minor salivary glands of all study groups. Also, a significantly different immune response to virus infection (protein IFI16, interferons gamma and beta, dendritic cells, and receptor for natural killers) was revealed in the minor salivary glands of the study groups. Cytometric analysis of the blood cells revealed a dropping amount of circulating natural killers and dendritic cells in patients with SS. Significant correlations between immunohistochemical staining and serological findings were revealed. Conclusions Abundant immunohistochemical signs of mumps virus protein in the salivary glands and depletion of circulating immune cells make a background for thought of presumable mumps or/and other virus participation in epithelial damage causing sicca syndrome in predisposed patients.

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“…However, the effects of type I IFNs in Sjögren’s syndrome may be subtype specific. IFN-β may reduce the expression of proinflammatory mediators in peripheral blood mononuclear cells isolated from patients with Sjögren’s syndrome 60. Like SLE, patients with Sjögren’s syndrome can be stratified by those who do and do not have an IFNGS.…”

Section: Type I Ifns In Autoimmune Diseasesmentioning

confidence: 99%

Type I interferons in host defence and inflammatory diseases

Crow

Rönnblom

2019

Lupus Sci Med

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Type I interferons (IFN) can have dual and opposing roles in immunity, with effects that are beneficial or detrimental to the individual depending on whether IFN pathway activation is transient or sustained. Determinants of IFN production and its functional consequences include the nature of the microbial or nucleic acid stimulus, the type of nucleic acid sensor involved in inducing IFN, the predominant subtype of type I IFN produced and the immune ecology of the tissue at the time of IFN expression. When dysregulated, the type I IFN system drives many autoimmune and non-autoimmune inflammatory diseases, including SLE and the tissue inflammation associated with chronic infection. The type I IFN system may also contribute to outcomes for patients affected by solid cancers or myocardial infarction. Significantly more research is needed to discern the mechanisms of induction and response to type I IFNs across these diseases, and patient endophenotyping may help determine whether the cytokine is acting as ‘friend’ or ‘foe’, within a particular patient, and at the time of treatment. This review summarises key concepts and discussions from the second International Summit on Interferons in Inflammatory Diseases, during which expert clinicians and scientists evaluated the evidence for the role of type I IFNs in autoimmune and other inflammatory diseases.

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Interferon-β inhibits inflammatory responses mediators via suppression of iNOS signaling pathway in PBMCs from patients with primary Sjögren’s syndrome

Abstract: Our findings highlight a consistent ex vivo inhibitory effect of IFN-β on pro-inflammatory cytokine production and NO pathway in pSS patients. Our data suggest that IFN-β could represent a potential candidate for targeting inflammation during pSS.

Cited by 8 publications

References 40 publications

Mesenchymal stem cell transplantation alleviates experimental Sjögren's syndrome through IFN-β/IL-27 signaling axis

Mesenchymal stem cell transplantation alleviates experimental Sjögren's syndrome through IFN-β/IL-27 signaling axis

Sjögren’s Syndrome: Concerted Triggering of Sicca Conditions

Type I interferons in host defence and inflammatory diseases

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