scholarly journals Clinical and Pathological Roles of Ro/SSA Autoantibody System

2012 ◽  
Vol 2012 ◽  
pp. 1-12 ◽  
Author(s):  
Ryusuke Yoshimi ◽  
Atsuhisa Ueda ◽  
Keiko Ozato ◽  
Yoshiaki Ishigatsubo
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Autoimmune Diseases ◽  
Lupus Erythematosus ◽  
Clinical Importance ◽  
Systemic Lupus ◽  
Systemic Autoimmune Diseases ◽  
Nuclear Antigens ◽  
Diagnosis And Classification

Anti-Ro/SSA antibodies are among the most frequently detected autoantibodies against extractable nuclear antigens and have been associated with systemic lupus erythematosus (SLE) and Sjögren's syndrome (SS). Although the presence of these autoantibodies is one of the criteria for the diagnosis and classification of SS, they are also sometimes seen in other systemic autoimmune diseases. In the last few decades, the knowledge of the prevalence of anti-Ro/SSA antibodies in various autoimmune diseases and symptoms has been expanded, and the clinical importance of these antibodies is increasing. Nonetheless, the pathological role of the antibodies is still poorly understood. In this paper, we summarize the milestones of the anti-Ro/SSA autoantibody system and provide new insights into the association between the autoantibodies and the pathogenesis of autoimmune diseases.

scholarly journals Role of MHC-Linked Susceptibility Genes in the Pathogenesis of Human and Murine Lupus

2012 ◽  
Vol 2012 ◽  
pp. 1-15 ◽  
Author(s):  
Manfred Relle ◽  
Andreas Schwarting
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Erythematosus ◽  
Association Studies ◽  
Susceptibility Genes ◽  
Genome Wide Association Studies ◽  
Systemic Lupus ◽  
Nuclear Antigens ◽  
Genome Wide ◽  
Conventional Drug

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by the production of autoantibodies against nuclear antigens and a systemic inflammation that can damage a broad spectrum of organs. SLE patients suffer from a wide variety of symptoms, which can affect virtually almost any tissue. As lupus is difficult to diagnose, the worldwide prevalence of SLE can only be roughly estimated to range from 10 and 200 cases per 100,000 individuals with dramatic differences depending on gender, ethnicity, and location. Although the treatment of this disease has been significantly ameliorated by new therapies, improved conventional drug therapy options, and a trained expert eye, the underlying pathogenesis of lupus still remain widely unknown. The complex etiology reflects the complex genetic background of the disease, which is also not well understood yet. However, in the past few years advances in lupus genetics have been made, notably with the publication of genome-wide association studies (GWAS) in humans and the identification of susceptibility genes and loci in mice. This paper reviews the role of MHC-linked susceptibility genes in the pathogenesis of systemic lupus erythematosus.

The essential role of costimulatory molecules in systemic lupus erythematosus

Lupus ◽  
2019 ◽  
Vol 28 (5) ◽  
pp. 575-582 ◽  
Author(s):  
Z X Xiao ◽  
N Olsen ◽  
S G Zheng
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Autoimmune Diseases ◽  
Lupus Erythematosus ◽  
Biological Effects ◽  
Critical Role ◽  
Chronic Inflammatory Disease ◽  
Costimulatory Molecules ◽  
Systemic Lupus ◽  
System Disorder

Systemic lupus erythematosus (SLE) is a chronic inflammatory disease with immune system disorder mediated through complex autoimmune pathways that involve immune cells, nonimmune cells, cytokines, chemokines, as well as costimulatory molecules. Costimulatory signals play a critical role in initiating, maintaining and regulating immune reactions, and these include ligands and receptors and their interactions involving multiple types of signal information. Dysfunction of costimulatory factors results in complicated abnormal immune responses, with biological effects and eventually, clinical autoimmune diseases. Here we outline what is known about various roles that costimulatory families including the B7 family and tumor necrosis factor super family play in SLE. The aim of this review is to understand the possible association of costimulation with autoimmune diseases, especially SLE, and to explore possible therapeutic target(s) of costimulatory molecules and pathways that might be used to develop therapeutic approaches for patients with these conditions.

The curious case of miR-155 in SLE

2021 ◽  
Vol 23 ◽  
Author(s):  
S. A. Ibrahim ◽  
A. Y. Afify ◽  
I. O. Fawzy ◽  
N. El-Ekiaby ◽  
A. I. Abdelaziz
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Immune System ◽  
Targeted Therapy ◽  
Animal Models ◽  
Autoimmune Diseases ◽  
Lupus Erythematosus ◽  
Systemic Lupus ◽  
Recent Attention ◽  
Made In

Abstract Epigenetic modifications have been well documented in autoimmune diseases. MicroRNAs (miRNAs), in particular, have long intrigued scientists in the field of autoimmunity. Owing to its central role in the development of the immune system, microRNA-155 (miR-155) is deeply involved in systemic lupus erythematosus (SLE). Despite the advancements made in treating SLE, the disease still remains incurable. Therefore, recent attention has been drawn to the manipulation of epigenetics in the development of curative treatments. In fact, it is a widely held view that miRNA-targeted therapy is a new glimmer of hope in the treatment of autoimmune diseases. However, the duplicity of miRNAs should not be overlooked. A single miRNA can target several mRNAs, and some mRNAs may possess opposing functions. In this review, we highlight the role of miR-155 as a biomarker and review its functions in SLE patients and animal models while discussing possible reasons behind inconsistencies across studies.

scholarly journals Signaling Pathways of Type I and Type III Interferons and Targeted Therapies in Systemic Lupus Erythematosus

Cells ◽  
2019 ◽  
Vol 8 (9) ◽  
pp. 963 ◽  
Author(s):  
I-Tsu Chyuan ◽  
Hong-Tai Tzeng ◽  
Ji-Yih Chen
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Autoimmune Diseases ◽  
Signaling Pathways ◽  
Lupus Erythematosus ◽  
Janus Kinase ◽  
Type I ◽  
Systemic Lupus ◽  
Type Iii ◽  
Signature Genes

Type I and type III interferons (IFNs) share several properties in common, including the induction of signaling pathways, the activation of gene transcripts, and immune responses, against viral infection. Recent advances in the understanding of the molecular basis of innate and adaptive immunity have led to the re-examination of the role of these IFNs in autoimmune diseases. To date, a variety of IFN-regulated genes, termed IFN signature genes, have been identified. The expressions of these genes significantly increase in systemic lupus erythematosus (SLE), highlighting the role of type I and type III IFNs in the pathogenesis of SLE. In this review, we first discussed the signaling pathways and the immunoregulatory roles of type I and type III IFNs. Next, we discussed the roles of these IFNs in the pathogenesis of autoimmune diseases, including SLE. In SLE, IFN-stimulated genes induced by IFN signaling contribute to a positive feedback loop of autoimmunity, resulting in perpetual autoimmune inflammation. Based on this, we discussed the use of several specific IFN blocking strategies using anti-IFN-α antibodies, anti-IFN-α receptor antibodies, and IFN-α-kinoid or downstream small molecules, which intervene in Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathways, in clinical trials for SLE patients. Hopefully, the development of novel regimens targeting IFN signaling pathways will shed light on promising future therapeutic applications for SLE patients.

Advances in the diagnosis and classification of systemic lupus erythematosus

2016 ◽  
Vol 12 (12) ◽  
pp. 1309-1320 ◽  
Author(s):  
Maddalena Larosa ◽  
Luca Iaccarino ◽  
Mariele Gatto ◽  
Leonardo Punzi ◽  
Andrea Doria
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Erythematosus ◽  
Systemic Lupus ◽  
Diagnosis And Classification
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