Immunometabolic Pathways and Its Therapeutic Implication in Autoimmune Diseases

Systemic Autoimmune Diseases

Immunometabolism in systemic lupus erythematosus: Relevant pathogenetic mechanisms and potential clinical applications

Thanks to advances in research, it may soon be easier to diagnose autoimmune diseases earlier, but therapy remains a tricky problem

Autoimmune diseases are diseases caused by tissue damage caused by the body's immune response to autoantibodies. Circular RNAs (CircRNAs) are a kind of special endogenous non-coding RNA that play a biological role by regulating gene transcription. In this work, we searched the PubMed, Web of Science (SCIE), National Science and Technology Library (NSTL), and ScienceDirect Online (SDOL) databases to summarize the impact of circRNAs on autoimmune diseases, especially the results of circRNAs in rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). The study on the function of circRNAs and autoimmune diseases further deepened our understanding of the development and pathogenesis of autoimmune diseases. CircRNAs may act as miRNA sponges to regulate biological processes and affect the occurrence and development of autoimmune diseases. CircRNAs are closely related to the pathogenesis of RA and SLE and may become potential biomarkers for the diagnosis and treatment of RA and SLE. CircRNAs play an important role in the pathogenesis of RA, SLE and other autoimmune diseases, and are expected to provide new biomarkers for the diagnosis and treatment of autoimmune diseases. However, the function and mechanism of circRNAs in autoimmune diseases need more comprehensive research.

Altered glucose metabolism in B cells: Implications for the pathogenesis and treatment of autoimmune diseases.

Background:Autoimmune diseases encompass a wide array of conditions characterized primarily by immune dysregulation, comprising hundreds of distinct diseases. However, the pathogenic mechanisms of systemic autoimmune diseases such as systemic lupus...

Research progress of single-cell transcriptome sequencing in autoimmune diseases and autoinflammatory disease: A review

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Systemic autoimmune diseases are a group of common diseases, including rheumatoid arthritis, systemic lupus erythematosus, spondyloarthropathy, Sjogren's syndrome, polymyositis, and dermatomyositis, etc. They are one of the leading causes of death and disability. With the use of glucocorticoid, immune suppression drugs and new developed biologics, the outcome of this group of diseases has greatly improved, but there is still no cure for them. Knowledge of the pathogenesis, diagnosis, and treatment of those diseases will lead to better understanding of the diseases and better care of patients. Based on this background, we assembled this special issue for a better understanding of the molecular pathology underlying systemic autoimmune diseases, the development of strategies to treat these conditions, and the evaluation of outcomes. In this special issue, several review articles discussed many important aspects about autoimmune disease. A. Mastrangelo et al. discussed the role of posttranslational protein modifications in rheumatoid arthritis. C. Gluhovschi et al. made a review about pregnancy associated with systemic lupus erythematosus. A. Kronbichler et al. reviewed the influence and role of microbial factors in autoimmune kidney diseases. T. Shizuma summarized clinical characteristics of concomitant systemic lupus erythematosus and primary biliary cirrhosis. Z. Wu and H. Nakanishi discussed the link between inflammatory bone disorders and Alzheimer's disease. K. R. Sigdel et al. made a review about the functions of long noncoding RNA in immune cells. L. Duan et al. made a review about treatment of bullous systemic lupus erythematosus. R. Hage-Sleiman et al. reviewed recent studies about the novel PKCtheta. L. Zhang et al. made a meta-analysis about interleukin-23R rs7517847 T/G polymorphism and the risk of Crohn's disease in Caucasians. Beside reviews, many original research studies about the pathogenesis or clinical characteristics of autoimmune disease were also included in this special issue. T. Elisa et al. studied the role of endothelin receptors in the pathogenesis of systemic sclerosis. A. Barbieri et al. analyzed the characterization of CD30/CD30L+ cells in peripheral blood and synovial fluid of patients with rheumatoid arthritis. G. F. Dong et al. researched the effect of leflunomide on the lipid rafts expression in SLE patients. P. Žigon et al. found that anti-phosphatidylserine/prothrombin antibodies were associated with adverse pregnancy outcomes. G. Sudzius et al. studied the distribution of peripheral lymphocyte populations in primary Sjogren's syndrome patients. J. Xu et al. showed that autoantibodies affect brain density reduction in nonneuropsychiatric systemic lupus erythematosus patients. B. Shen et al. found that body image disturbances have impact on the sexual problems in systemic lupus erythematous patients. G. Guo et al. and C. Zhao et al. studied mesenchymal stem cells in SLE and RA patients. Y. Liu et al. found a new serological marker in SLE patients. A. E. Ngono et al. found that frequency of circulating myelin oligodendrocyte glycoprotein B lymphocytes was decreased in relapsing-remitting multiple sclerosis patients. J. Amaya-Amaya et al. showed that GDF15 (MIC1) H6D polymorphism does not influence cardiovascular disease in a Latin American population with rheumatoid arthritis. A. D. Rocha-Munoz et al. demonstrated that anti-CCP2 antibodies are markers associated with the severity of RA- ILD. M. Lu et al. found that HMGB1 promoted systemic lupus erythematosus by enhancing macrophage inflammatory response. A. D. Rocha-Munoz et al. studied the influence of anti-TNF and disease modifying antirheumatic drugs (DMARDs) therapy on pulmonary forced vital capacity associated with ankylosing spondylitis. B. Kisiel et al. showed that methotrexate, cyclosporine A, and biologics protect against atherosclerosis in rheumatoid arthritis. L. Wang et al. analyzed clinical characteristics of cerebral venous sinus thrombosis in SLE patients. This special issue covers many important aspects in autoimmune diseases, which will surely provide us with a better understanding about the pathogenesis, diagnosis, and treatment of autoimmune diseases. Guixiu Shi Jianying Zhang Zhixin (Jason) Zhang Xuan Zhang

Advances in autoimmune rheumatic diseases

To describe the frequency of polyautoimmunity and multiple autoimmune syndrome in patients with rheumatoid arthritis (RA) and patients with systemic lupus erythematosus (SLE). This was a cross-sectional observational study of patients with RA, SLE, and controls without autoimmune rheumatic disease. Cases were those with RA according to the 2010 American College of Rheumatology/European League Against Rheumatism criteria and SLE according to the 2019 American College of Rheumatology/European League Against Rheumatism criteria, consecutively recruited in a rheumatology clinic. Controls were subjects with no rheumatic autoimmune disease (AIDs) recruited in the same area. Patients filled out a questionnaire on polyautoimmunity. Variables of interest were polyautoimmunity (RA or SLE with other AIDs), whereas secondary variables were rheumatic, skin, endocrine, digestive, and neurological AIDs. Multiple autoimmune syndrome is defined as the presence of 3 or more AIDs and a family history of AIDs. Statistical analyses performed were descriptive, bivariate, and multivariate (dependent variable: polyautoimmunity). The study population comprised 109 patients with RA, 105 patients with SLE, and 88 controls. Polyautoimmunity was recorded in 15 patients with RA (13.8%), 43 with SLE (41%), and 2 controls (2.2%). The most frequent AID in RA was Sjögren syndrome (53.3%), followed by Hashimoto thyroiditis and psoriasis; the most frequent AIDs in SLE were Sjögren syndrome (55.8%) and antiphospholipid syndrome (30.2%), followed by Hashimoto thyroiditis. Obesity was associated with polyautoimmunity in RA (odds ratio [OR], 3.362; p = 0.034). In SLE, joint damage (OR, 2.282; p = 0.038) and anti-RNP antibodies (OR, 5.095; p = 0.028) were risk factors for polyautoimmunity, and hydroxychloroquine was a protective factor (OR, 0.190; p = 0.004). Polyautoimmunity is frequent in RA and even more frequent in SLE. It was associated with obesity in RA and with joint damage and anti-RNP in SLE. Hydroxychloroquine was a protector.

Systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) are two common multisystem autoimmune diseases that share, among others, many clinical manifestations and serological features. The role of long non-coding RNAs (lncRNAs) has been of particular interest in the pathogenesis of autoimmune diseases. Here, we aimed to summarize the roles of lncRNAs as emerging novel biomarkers and therapeutic targets in SLE and RA. We conducted a narrative review summarizing original articles on lncRNAs associated with SLE and RA, published until November 1, 2021. Based on the studies on lncRNA expression profiles in samples (including PBMCs, serum, and exosomes), it was noted that most of the current research is focused on investigating the regulatory mechanisms of these lncRNAs in SLE and/or RA. Several lncRNAs have been hypothesized to play key roles in these diseases. In SLE, lncRNAs such as GAS5, NEAT1, TUG1, linc0949, and linc0597 are dysregulated and may serve as emerging novel biomarkers and therapeutic targets. In RA, many validated lncRNAs, such as HOTAIR, GAS5, and HIX003209, have been identified as promising novel biomarkers for both diagnosis and treatment. The shared lncRNAs, for example, GAS5, may participate in SLE pathogenesis through the mitogen-activated protein kinase pathway and trigger the AMP-activated protein kinase pathway in RA. Here, we summarize the data on key lncRNAs that may drive the pathogenesis of SLE and RA and could potentially serve as emerging novel biomarkers and therapeutic targets in the coming future.

The emerging roles of exosomes in autoimmune diseases, with special emphasis on microRNAs in exosomes

Autoimmune diseases have several etiologies. Acute Chlamydia pneumoniae (C. pneumoniae) infection may be involved in the pathogenesis of several autoimmune diseases. In this study, 82 patients with several autoimmune diseases and 70 controls were enrolled, and acute C. pneumoniae infection has been evaluated by monitoring the levels of IgM antibody. Chlamydia pneumoniae IgM positive results were observed in 29% (P < 0.05) of the patients with several autoimmune diseases and in 10% of the controls. Chlamydia pneumoniae IgM positive cases were more frequent among the patients with rheumatoid arthritis (RA; 30%, P < 0.05), systemic lupus erythematosus (SLE; 28.0%, P < 0.05), dermatomyositis/polymyositis (23%, NS), myeloperoxidase-antineutrophil cytoplasmic autoantibody (MPO-ANCA)-associated vasculitis (33%, NS), adult onset of Still's disease (29%, NS) and giant cell arteritis/Takayasu arteritis (50%, NS) than among the controls. This positive frequency was statistically significant in RA and SLE. These results suggest that acute C. pneumoniae infection is probably involved in the pathogenesis of autoimmune diseases.

Nowadays, autoimmune diseases(AD) still torment many people and they always suffer from severe symptoms and complications. However, the pathogenesis of AD is still unclear and needs more research. Also, there are shortages of treatments which can totally cure AD. This research mainly focuses on current findings of possible pathogenesis and treatments for AD by discussing and analyzing two of most famous AD: rheumatoid arthritis and systemic lupus erythematosus (SLE). This essay discusses pathogenesis of RA and SLE from three aspects: genes, immune systems and environmental factors, and then concludes current medications and therapies as well as their drawbacks. This study finds that susceptible genes, abnormal immune responses and environmental stimulation can synergistically lead to autoimmune diseases, and existing treatments are mainly composed of symptomatic treatments and modifying treatments. But each medication has its inevitable side effects. Furthermore, more research should focus on systematic treatments with fewer drawbacks in order to truly cure AD.