Type I IFN signature in primary Sjögren’s syndrome patients

Brkić, Zana; Versnel, Marjan A.

doi:10.1586/1744666x.2014.876364

Cited by 38 publications

(26 citation statements)

References 101 publications

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“…Similarly, elimination of the type 1 interferon receptor, or interferon itself, was shown to eliminate multiple features of SS, supporting the notion promoted in human studies on SS that type 1 interferon is a major driver of disease pathogenesis in SS [50,51,52,53]. …”

Section: Potential Roles For B Cells In Sjogren’s Syndromesupporting

confidence: 56%

Multiple Roles for B-Lymphocytes in Sjogren’s Syndrome

Ambrus

Peck

2016

JCM

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Sjogren’s syndrome (SS) is a complex heterogeneous autoimmune disease resulting in loss of salivary gland and lacrimal gland function that may include multiple systemic manifestations including lymphoma. Multiple cell types participate in disease pathogenesis. This review discusses evidence for abnormal B cell subpopulations in patients with SS, critical roles of B cells in SS and the status of B cell–directed therapies in the management of patients with SS.

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Section: Potential Roles For B Cells In Sjogren’s Syndromesupporting

confidence: 56%

Multiple Roles for B-Lymphocytes in Sjogren’s Syndrome

Ambrus

Peck

2016

JCM

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“…The clinical presentation of different AID varies, but evidence from genome-wide association studies points toward common immunogenetic mechanisms, as many systemic AID share disease-associated genes (231). Another trait particularly shared amongst different antibody-driven AID is the expression of a T1-IFN signature in both blood- and disease-affected tissue (232–234), the strength of which generally correlates with disease activity and severity (235–238). Vice versa , T1-IFN immunotherapy as treatment for other diseases is known to cause symptoms similar to those observed in AID, such as development of psoriatic lesions in MS or hepatitis C-infected patients (239, 240).…”

Section: T1-ifns the Th17 Response And Their Interactions In Autoimmmentioning

confidence: 99%

Interactions between Type 1 Interferons and the Th17 Response in Tuberculosis: Lessons Learned from Autoimmune Diseases

et al. 2017

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The classical paradigm of tuberculosis (TB) immunity, with a central protective role for Th1 responses and IFN-γ-stimulated cellular responses, has been challenged by unsatisfactory results of vaccine strategies aimed at enhancing Th1 immunity. Moreover, preclinical TB models have shown that increasing IFN-γ responses in the lungs is more damaging to the host than to the pathogen. Type 1 interferon signaling and altered Th17 responses have also been associated with active TB, but their functional roles in TB pathogenesis remain to be established. These two host responses have been studied in more detail in autoimmune diseases (AID) and show functional interactions that are of potential interest in TB immunity. In this review, we first identify the role of type 1 interferons and Th17 immunity in TB, followed by an overview of interactions between these responses observed in systemic AID. We discuss (i) the effects of GM-CSF-secreting Th17.1 cells and type 1 interferons on CCR2+ monocytes; (ii) convergence of IL-17 and type 1 interferon signaling on stimulating B-cell activating factor production and the central role of neutrophils in this process; and (iii) synergy between IL-17 and type 1 interferons in the generation and function of tertiary lymphoid structures and the associated follicular helper T-cell responses. Evaluation of these autoimmune-related pathways in TB pathogenesis provides a new perspective on recent developments in TB research.

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“…There are scarcely no studies determining the eNOS function and NO generation in pSS. However, some recent data shows increased oxidative stress in pSS and association of disease with IFN-I signature, which could exert indirect effects as described above [174][175][176]. Therefore, pSS emerges due to the similarity to SLE and RA and also due to the fact that most patients are out on medication, as an interesting model to study atherosclerosis in autoimmune diseases.…”

Section: Primary Sjogren Syndrome (Pss)mentioning

confidence: 99%

Role of the eNOS Uncoupling and the Nitric Oxide Metabolic Pathway in the Pathogenesis of Autoimmune Rheumatic Diseases

Łuczak

Madej

Kasprzyk

et al. 2020

Oxidative Medicine and Cellular Longevity

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Atherosclerosis and its clinical complications constitute the major healthcare problems of the world population. Due to the central role of endothelium throughout the atherosclerotic disease process, endothelial dysfunction is regarded as a common mechanism for various cardiovascular (CV) disorders. It is well established that patients with rheumatic autoimmune diseases are characterized by significantly increased prevalence of cardiovascular morbidity and mortality compared with the general population. The current European guidelines on cardiovascular disease (CVD) prevention in clinical practice recommend to use a 1,5-factor multiplier for CV risk in rheumatoid arthritis as well as in other autoimmune inflammatory diseases. However, mechanisms of accelerated atherosclerosis in these diseases, especially in the absence of traditional risk factors, still remain unclear. Oxidative stress plays the major role in the endothelial dysfunction and recently is strongly attributed to endothelial NO synthase dysfunction (eNOS uncoupling). Converted to a superoxide-producing enzyme, uncoupled eNOS not only leads to reduction of the nitric oxide (NO) generation but also potentiates the preexisting oxidative stress, which contributes significantly to atherogenesis. However, to date, there are no systemic analyses on the role of eNOS uncoupling in the excess CV mortality linked with autoimmune rheumatic diseases. The current review paper addresses this issue.

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Type I IFN signature in primary Sjögren’s syndrome patients

Cited by 38 publications

References 101 publications

Multiple Roles for B-Lymphocytes in Sjogren’s Syndrome

Multiple Roles for B-Lymphocytes in Sjogren’s Syndrome

Interactions between Type 1 Interferons and the Th17 Response in Tuberculosis: Lessons Learned from Autoimmune Diseases

Role of the eNOS Uncoupling and the Nitric Oxide Metabolic Pathway in the Pathogenesis of Autoimmune Rheumatic Diseases

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