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This article discusses a literature search that was conducted to identify the top 100 cited papers in cutaneous lupus erythematosus (CLE). CLE is a subset of lupus erythematosus characterized by autoimmune-mediated skin manifestations. The search yielded 5750 articles, and the top 100 most cited articles were categorized into basic science research, clinical research, or new treatment categories. The majority of the top cited articles were clinical research articles, indicating their impact on research and clinical practice. The findings reveal important contributions to understanding CLE's pathogenesis, epidemiology, and management, providing valuable insights for researchers, clinicians, and funders in the field of autoimmune skin disorders. [Extracted from the article]

Moderate-to-severe psoriasis is associated with significant comorbidity, an impaired quality of life, and increased medical costs, including those associated with treatments. Systematic reviews (SRs) and meta-analyses (MAs) of randomized clinical trials are considered two of the best approaches to the summarization of high-quality evidence. However, methodological bias can reduce the validity of conclusions from these types of studies and subsequently impair the quality of decision making. As co-authorship is among the most well-documented forms of research collaboration, the present study aimed to explore whether authors’ collaboration methods might influence the methodological quality of SRs and MAs of psoriasis. Methodological quality was assessed by two raters who extracted information from full articles. After calculating total and per-item Assessment of Multiple Systematic Reviews (AMSTAR) scores, reviews were classified as low (0-4), medium (5-8), or high (9-11) quality. Article metadata and journal-related bibliometric indices were also obtained. A total of 741 authors from 520 different institutions and 32 countries published 220 reviews that were classified as high (17.2%), moderate (55%), or low (27.7%) methodological quality. The high methodological quality subnetwork was larger but had a lower connection density than the low and moderate methodological quality subnetworks; specifically, the former contained relatively fewer nodes (authors and reviews), reviews by authors, and collaborators per author. Furthermore, the high methodological quality subnetwork was highly compartmentalized, with several modules representing few poorly interconnected communities. In conclusion, structural differences in author-paper affiliation network may influence the methodological quality of SRs and MAs on psoriasis. As the author-paper affiliation network structure affects study quality in this research field, authors who maintain an appropriate balance between scientific quality and productivity are more likely to develop higher quality reviews. [ABSTRACT FROM AUTHOR]

Primary immunodeficiency diseases (PIDs) caused by a single-gene defect generally are referred to as monogenic autoimmune disorders. For example, mutations in the transcription factor autoimmune regulator (AIRE) result in a condition called autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy; while mutations in forkhead box P3 lead to regulatory T cell (Treg)-deficiency-induced multiorgan inflammation, which in humans is called "immune dysregulation, polyendocrinopathy, enteropathy with X-linked inheritance" (or IPEX syndrome). Previous studies concluded that monogenic diseases are insensitive to commensal microbial regulation because they develop even in germ-free (GF) animals, a conclusion that has limited the number of studies determining the role of microbiota in monogenic PIDs. However, emerging evidence shows that although the onset of the disease is independent of the microbiota, several monogenic PIDs vary in severity in association with the microbiome. In this review, we focus on monogenic PIDs associated with Treg deficiency/dysfunction, summarizing the gut microbial dysbiosis that has been shown to be linked to these diseases. From limited studies, we have gleaned several mechanistic insights that may prove to be of therapeutic importance in the early stages of life. IMPACT: This review paper serves to refute the concept that monogenic PIDs are not linked to the microbiome. The onset of monogenic PIDs is independent of microbiota; single-gene mutations such as AIRE or Foxp3 that affect central or peripheral immune tolerance produce monogenic diseases even in a GF environment. However, the severity and outcome of PIDs are markedly impacted by the microbial composition. We suggest that future research for these conditions may focus on targeting the microbiome., (© 2021. The Author(s), under exclusive licence to the International Pediatric Research Foundation, Inc.)

Background: Sponsors that seek to commercialize new drugs apply to the Food and Drug Administration (FDA) which independently analyzes the raw data and reports the results on its website. Objectives: This study sought to determine if there are differences between the FDA assessments and journal reports on biologic agents developed for the treatment of rheumatoid arthritis. Methods: Available data on FDA-approved drugs were extracted from the website, and a systematic literature search was conducted to identify matching studies in peer-reviewed medical journals. Outcome measures were the American College of Rheumatology response criteria ACR20 (efficacy) and withdrawal due to adverse events (safety). As effect size odds ratios were estimated for each active trial arm vs. control arm (i.e. for both sources: FDA and journal report), followed by calculation of the ratios of the FDA and journal report odds ratios. A ratio of odds ratios not equal to 1 was categorized as a discrepancy. Results: FDA reports were available for 8 of 9 FDA-approved biologic agents for rheumatoid arthritis; all identified trials (34) except one were published in peer-reviewed journals. Overall, discrepancies were noted for 20 of the 33 evaluated trials. Differences in the apparent benefit reporting were found in 39% (24/61) pairwise comparisons and in 11 cases these were statistically significant; the FDA report showed greater benefit than the journal publication in 15 comparisons and lesser benefit in 9. Differences in the reported harms were found in 51% (28/55) pairwise comparisons and were statistically significant in 5. The “signal” in FDA reports showed a less harmful effect than the journal publication in 17 comparisons whereas a more harmful effect in 11. The differences were attributed to differences in analytic approach, patient inclusion, rounding effect, and counting discrepancies. However, no differences were categorized as critical. Conclusion: There was no empirical evidence to suggest biased estimates between the two sources. Increased and detailed transparency in publications would improve the understanding and credibility of published results. Further, the FDA report was found to be a useful source when data are missing in the published report (i.e. reporting bias). [ABSTRACT FROM AUTHOR]

Advanced Therapy Medicinal Products (ATMPs) are innovative and complex medicines which can potentially be used to treat a variety of human health issues, including cancers (such as leukemia and melanoma), neurodegenerative diseases (such as Huntington's and Parkinson's diseases), inherited diseases and autoimmune diseases (such as diabetes, multiple sclerosis and rheumatoid arthritis). They are particularly important for severe, rare, or chronic diseases where conventional approaches have proven to be inadequate. The number of patients treated with specific ATMPs, however, is still very low. The League of European Research Universities (LERU) is a well-established network of research-intensive universities. They develop and disseminate their views on research, innovation and higher education through policy papers, statements, meetings and events helping to shape policy at the EU level. Universities already play an important role in ATMP development, but their role could be improved, made larger and more prominent, if specific hurdles were addressed. In this paper, we outline possible ways in which this could be done. Ways in which ATMP development at universties and patient access to these products can be improved include: 1) Improving interactions with, and help provided by, support organisations, such as EMA, industry and other universities, to cover better the whole product development pathway and to ensure support (including financial) at all stages of development. 2) Focusing on new innovative products that address an unmet medical need and have a high chance of success but which are unlikely to be attractive to industry. 3) Retaining the Hospital Exemption, but harmonising its application and improving its assessment, and using it only in product development or for products not suitable for Marketing Authorisation. A registry should be developed to record information on ATMP use under the Hospital Exemption. 4) Improving transparency, both in ATMP trials and in the use of the Hospital Exemption, which will help organisations active in this field to learn from others' successes and failures. LERU hopes that the actions in this paper will lead to the development of new therapeutic options, improved links with the pharmaceutical industry and, most importantly, to better patient access to these innovative medicinal products. [ABSTRACT FROM AUTHOR]

In the first paper [[10]], the epidemiologic, clinical, and immunological features of CVID-associated giardiasis are reviewed, evidencing that patients with giardiasis more commonly have reduced IgA levels and lower levels of switched memory B cells. 35566429 12 Pieniawska-'Smiech K., Kuraszewicz A., Sado J., 'Smiech K., Lewandowicz-Uszy'nska A. Assessment of COVID-19 Incidence and the Ability to Synthesise Anti-SARS-CoV-2 Antibodies of Paediatric Patients with Primary Immunodeficiency. The atypical presentation of IEI is also the main focus of the paper by Morawska et al., which explores the spectrum of atopic manifestations in patients with selective IgA deficiency (sIgAD). This work analyzes the most common autoimmune manifestations in patients with antibody deficiencies, combined immunodeficiencies, and immune dysregulation disorders, and also introduces some specific monogenic entities that are used as a paradigm of "druggable" IEI. [Extracted from the article]

Introduction and aim. Treatment with bisphosphonates (BPs) has many advantages, low risk of side effects, and relatively low cost of treatment. In addition, bisphosphonates can be used in patients of all ages, which is especially important in the case of older people, in whom osteoporosis is a common condition. Bisphosphonates are a group of drugs used to treat rheumatic diseases, including osteoporosis, Paget's disease, as well as autoimmune diseases, such as systemic lupus erythematosus or arthritis. The mechanism of action of bisphosphonates is to inhibit the activity of osteoclasts, cells responsible for bone resorption, which leads to inhibition of bone loss and a reduction in the risk of fractures. Material and methods. Review of the current literature was conducted using PubMed, ScienceDirect and Google Scholar. Analysis of literature. Zoledronate modulates the cytotoxic T-lymphocyte antigen-4 (CTLA-4). The function of CTLA-4 is to attenuate the ongoing immune response. Treatment of rheumatoid arthritis, the addition of zoledronate to the therapy resulted in a reduction in the formation of new erosions in the joints of the hand and wrist. In the early therapy of spondyloarthropathies, BPs may be useful, as they reduce the level of proinflammatory cytokines and inhibit the activity of macrophages and osteoblasts. In addition, clinical symptoms will decrease, spine pain decreased or reductions of inflammatory changes in the spine in AS. SAPHO treatment with BPs showed a good response, although their effect was mainly based on anti-resorptive properties, they were shown to exert anti-inflammatory effects by modulating the activity of IL-1β, IL-6 and TNF-α. Conclusion. In conclusion is important to remember about the appropriate dose and duration of treatment, especially in patients with autoimmune diseases, as it may be necessary to use higher doses than recommended, what is associated with a higher risk of side effects such as allergic reactions, problems with the digestive tract or electrolyte disturbances and increased risk of hip fracture in patients using bisphosphonates for long periods of time. [ABSTRACT FROM AUTHOR]

Introduction and aim. Still's disease is a rare systemic inflammatory disease that is mediated by autoimmune processes. It's equivalent to juvenile idiopathic arthritis. The etiology of the disease is unknown. Description of the case. A 24-year-old patient was admitted to the Department of Rheumatology with suspicion of Still's disease. From 5 days before the admission, fever, sore throat, pains and swelling of the joints, a salmon-colored rash appeared. In laboratory tests, elevated CRP, leukocytosis with neutrophilia, anemia were observed, ferritin levels were above normal. Abdominal ultrasonography revealed hepatosplenomegaly. During the stay, recurring daily fevers in the evening were observed, with joint pain and itchy salmon-colored skin. Ultrasound of the lymph nodes was performed, revealing generalized lymphadenopathy. From the beginning of the stay, antibiotic therapy and metiprednisolone infusions were used, observing a temporary resolution of fever and in- flammatory parameters. The patient refused treatment with methotrexate, so cyclosporine was started. On the 10th day of stay recurrence of fever, increase in inflammatory parameters and ferritin were observed. Due to the unclear picture of the disease, a decision to start with prednisone was made. Gradual normalization of inflammatory parameters and improvement of the general condition were observed, but the fever persisted and the level of ferritin increased. Bone marrow puncture was performed. Quite numerous hemophagocytes were observed. Treatment with dexamethasone was initiated and the use of cyclosporine was resumed. General condition improved. Due to the observed steroid dependence, biological therapy was planned, which was postponed due to the positive result of the IGRA test so anti-mycobacterial prophylaxis was started. Then treatment with anakinra was started, resulting in remission of disease. Conclusion. Summing up, the patient was diagnosed with a drug-resistant form of Still's disease with a dangerous complication macrophage activation syndrome. However, the diagnosis of the disease is often problematic, which is mainly due to the lack of specific diagnostic markers. [ABSTRACT FROM AUTHOR]

Introduction and aim. Congenital heart block in fetus may occur when pregnant woman suffers from an autoimmune disease. The placenta transfers maternal antibodies specific for Ro and La autoantigens. The heart of fetus, which is anatomically correct, does not work in the proper way. The electrical conduction system of the heart is being inflamed, therefore it leads to electric signal detainment. This disorder is rare, and in every case it may be divergent and conduct to various manifestations. Description of the case. We present the course of medical diagnosis of a woman who is 29 years old, in her second pregnancy. Before gestation she didn't have a previous history of an rheumatic illness. Her laboratory results showed a high level of antibodies Ro and La, she had typical symptoms for an autoimmune disease. The fetus was diagnosed with bradycardia and first degree heart block at the 28th week of pregnancy. Conclusion. There is a popular opinion that all autoimmune diseases are always becoming muted during pregnancy. This case report is the exception to this rule. A characteristic manifestation of this autoimmune disease led to the correct diagnosis and proper therapy. [ABSTRACT FROM AUTHOR]

Background: Pediatric autoimmune neuropsychiatric disorders associated with streptococcus (PANDAS) is a controversial diagnosis with limited evidence-based treatment guidelines available, particularly for severe and treatment-resistant cases., Case Presentation: This report describes a 9-year-old male presenting with sudden onset, severe obsessive-compulsive disorder (OCD) symptoms one month following a streptococcus infection. His symptoms included suicidality and recurrent self-injurious behaviors, which led to multiple inpatient hospitalizations. He was diagnosed with PANDAS and was treated with psychotropic medications, antibiotics, immunotherapy, and a tonsillectomy. Over the two years since initial admission, the patient's condition improved, with a decrease in symptom severity and an increase in adaptive functioning, though symptom remission was slow to occur., Conclusions: This paper explores the controversies surrounding the PANDAS diagnosis, reviews potential treatments, and discusses the dilemmas of medical decision-making in the setting of severe treatment-resistant symptoms and limited evidence-based guidelines. We hope that this case report will be valuable to healthcare providers facing similar presentations and inspire further investigation into this complex condition., (© 2024. The Author(s).)

Autoimmune rheumatic diseases (ARD) present a significant global health challenge characterized by a rising prevalence. These highly heterogeneous diseases involve complex pathophysiological mechanisms, leading to variable treatment efficacies across individuals. This variability underscores the need for personalized and precise treatment strategies. Traditionally, clinical practices have depended on empirical treatment selection, which often results in delays in effective disease management and can cause irreversible damage to multiple organs. Such delays significantly affect patient quality of life and prognosis. Artificial intelligence (AI) has recently emerged as a transformative tool in rheumatology, offering new insights and methodologies. Current research explores AI's capabilities in diagnosing diseases, stratifying risks, assessing prognoses, and predicting treatment responses in ARD. These developments in AI offer the potential for more precise and targeted treatment strategies, fostering optimism for enhanced patient outcomes. This paper critically reviews the latest AI advancements for predicting treatment responses in ARD, highlights the current state of the art, identifies ongoing challenges, and proposes directions for future research. By capitalizing on AI's capabilities, researchers and clinicians are poised to develop more personalized and effective interventions, improving care and outcomes for patients with ARD., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Yang, Liu, Chen, Luo, Xu and Zhang.)

Background. Pathological changes in vitamin B12 levels are a common laboratory finding. The increase in serum vitamin B12 levels is termed B12 hypervitaminemia, often perceived as a benign disorder, leading to its underestimation. Objective.This paper aims to examine the potential pathogenetic mechanisms and the association of vitamin B12 excess with various diseases. Methodology. A literature search was conducted using the PubMed, DOAJ, and Google Scholar databases. The search was focused on original articles, review papers, and reference lists published in English since 2000. Results. Increased vitamin B12 levels are encountered in hematological disorders, solid tumors, renal and hepatic diseases, as well as inflammatory conditions. Vitamin B12 supplements increase the levels and can exacerbate underlying pathological conditions. The pathophysiology involves disturbances in the biology and metabolism of vitamin B12 and its carrier proteins. Falsely elevated values can arise due to interferences in quantitative assays. Elevated vitamin B12 may represent an incidental finding, accompany findings of underlying disease, and coexist with manifestations of functional deficiency. Conclusion. Elevated vitamin B12 may serve as an early indicator for the diagnosis and monitoring of serious diseases. Understanding the underlying pathogenetic mechanisms and establishing diagnostic algorithms are crucial areas for future research. [ABSTRACT FROM AUTHOR]

Autoimmune rheumatic diseases comprise a group of immune-related disorders characterized by non-organ-specific inflammation. These diseases include systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), ankylosing spondylitis (AS), gout, among others. Typically involving the hematologic system, these diseases may also affect multiple organs and systems. The pathogenesis of autoimmune rheumatic immune diseases is complex, with diverse etiologies, all associated with immune dysfunction. The current treatment options for this type of disease are relatively limited and come with certain side effects. Therefore, the urgent challenge remains to identify novel therapeutic targets for these diseases. Sterol regulatory element-binding proteins (SREBPs) are basic helix-loop-helix-leucine zipper transcription factors that regulate the expression of genes involved in lipid and cholesterol biosynthesis. The expression and transcriptional activity of SREBPs can be modulated by extracellular stimuli such as polyunsaturated fatty acids, amino acids, glucose, and energy pathways including AKT-mTORC and AMP-activated protein kinase (AMPK). Studies have shown that SREBPs play roles in regulating lipid metabolism, cytokine production, inflammation, and the proliferation of germinal center B (GCB) cells. These functions are significant in the pathogenesis of rheumatic and immune diseases (Graphical abstract). Therefore, this paper reviews the potential mechanisms of SREBPs in the development of SLE, RA, and gout, based on an exploration of their functions., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Xu, Jin, Chang and Ding.)

Background and Objectives : Vitamin D is a secosteroid hormone essential for calcium homeostasis and skeletal health, but established evidence highlights its significant roles also in muscle health and in the modulation of immune response. This review aims to explore the impact of impaired vitamin D status on outcomes of muscle function and involvement in inflammatory and autoimmune rheumatic diseases damaging the skeletal muscle efficiency both with direct immune-mediated mechanisms and indirect processes such as sarcopenia. Methods : A comprehensive literature search was conducted on PubMed and Medline using Medical Subject Headings (MeSH) terms: "vitamin D, muscle, rheumatic diseases." Additionally, conference abstracts from The European Alliance of Associations for Rheumatology (EULAR) and the American College of Rheumatology (ACR) (2020-2023) were reviewed, and reference lists of included papers were scanned. The review emphasizes the evidence published in the last five years, while also incorporating significant studies from earlier years, structured by the extent of evidence linking vitamin D to muscle health in the most commonly inflammatory and autoimmune rheumatic diseases encountered in clinical practice. Results : Observational studies indicate a high prevalence of vitamin D serum deficiency (mean serum concentrations < 10 ng/mL) or insufficiency (<30 ng/mL) in patients with idiopathic inflammatory myopathies (IIMs) and polymyalgia rheumatica, as well as other autoimmune connective tissue diseases such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE) and systemic sclerosis (SSc). Of note, vitamin D insufficiency may be associated with reduced muscle strength (2 studies on RA, 2 in SLE and 1 in SSc), increased pain (1 study on SLE), fatigue (2 studies on SLE), and higher disease activity (3 studies on IIMs and 1 on SLE) although there is much heterogeneity in the quality of evidence and different associations for the different investigated diseases. Therefore, linked to the multilevel biological intervention exerted by vitamin D, several translational and clinical studies suggest that active metabolites of this secosteroid hormone, play a role both in reducing inflammation, but also in enhancing muscle regeneration, intra-cellular metabolism and mitochondrial function, although interventional studies are limited. Conclusions : Altered serum vitamin D status is commonly observed in inflammatory and autoimmune rheumatic diseases and seems to be associated with adverse muscle health outcomes. While maintaining adequate serum vitamin D concentrations may confer muscle-protective effects, further research is needed to confirm these findings and establish optimal supplementation strategies to obtain a safe and efficient serum threshold.

The pathophysiology of several illnesses, including cancer and autoimmune diseasesdepends on human regulatory T cells (Tregs), and abnormalities in these cells may function as triggers for these conditions. Cancer and autoimmune, and gynecological diseases are associated with the differentiation of the proinflammatory T cell subset TH17 and its balance with the production of Treg. Recently, long non-coding RNAs (lncRNAs) have become important regulatory molecules in a wide range of illnesses. During epigenetic regulation, they can control the expression of important genes at several levels by affecting transcription, post-transcriptional actions, translation, and protein modification. They might connect with different molecules, such as proteins, DNA and RNA, and their structural composition is intricate. Because lncRNAs regulatebiological processes, including cell division, death, and growth, they are linked to severaldiseases. A notable instance of this is the lncRNA NEAT1, which has been the subject of several investigations to ascertain its function in immune cell development. In the context of immune cell development, several additional lncRNAs have been connected to Treg cell differentiation. In this work, we summarize current findings about the diverse functions of lncRNAs in Treg cell differentiation and control of the Th17/Treg homeostasis in autoimmune disorders, cancers, as well as several gynecological diseases where Tregs are key players., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024. Published by Elsevier Ltd.)

Background: The cyclic GMP-AMP synthase (cGAS)-stimulator of interferon (IFN) genes (STING) pathway is critical in the innate immune system and can be mobilized by cytosolic DNA. The various inflammatory and autoimmune diseases progression is highly correlated with aberrant cGAS-STING pathway activation. While some cGAS-STING pathway inhibitor were identified, there are no drugs that can be applied to the clinic. Compound Danshen Dripping Pill (CDDP) has been successfully used in clinic around the world, but the most common application is limited to cardiovascular disease. Therefore, the purpose of the present investigation was to examine whether CDDP inhibits the cGAS-STING pathway and could be used as a therapeutic agent for multiple cGAS-STING-triggered diseases., Methods: BMDMs, THP1 cells or Trex1 -/- BMDMs were stimulated with various cGAS-STING-agonists after pretreatment with CDDP to detect the function of CDDP on IFN-β and ISGs productionn. Next, we detect the influence on IRF3 and P65 nuclear translocation, STING oligomerization and STING-TBK1-IRF3 complex formation of CDDP. Additionally, the DMXAA-mediated activation mice model of cGAS-STING pathway was used to study the effects of CDDP. Trex1 -/- mice model and HFD-mediated obesity model were established to clarify the efficacy of CDDP on inflammatory and autoimmune diseases., Results: CDDP efficacy suppressed the IRF3 phosphorylation or the generation of IFN-β, ISGs, IL-6 and TNF-α. Mechanistically, CDDP did not influence the STING oligomerization and IRF3-TBK1 and STING-IRF3 interaction, but remarkably eliminated the STING-TBK1 interaction, ultimately blocking the downstream responses. In addition, we also clarified that CDDP could suppress cGAS-STING pathway activation triggered by DMXAA, in vivo. Consistently, CDDP could alleviate multi-organ inflammatory responses in Trex1 -/- mice model and attenuate the inflammatory disorders, incleding obesity-induced insulin resistance., Conclusion: CDDP is a specifically cGAS-STING pathway inhibitor. Furthermore, we provide novel mechanism for CDDP and discovered a clinical agent for the therapy of cGAS-STING-triggered inflammatory and autoimmune diseases., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier GmbH. All rights reserved.)

Autoimmune inner ear disease (AIED) is an organ-specific disease characterized by irreversible, prolonged, and progressive hearing and equilibrium dysfunctions. The primary symptoms of AIED include asymmetric sensorineural hearing loss accompanied by vertigo, aural fullness, and tinnitus. AIED is divided into primary and secondary types. Research has been conducted using animal models of rheumatoid arthritis (RA), a cause of secondary AIED. However, current models are insufficient to accurately analyze vestibular function, and the mechanism underlying the onset of AIED has not yet been fully elucidated. Elucidation of the mechanism of AIED onset is urgently needed to develop effective treatments. In the present study, we analyzed the pathogenesis of vertigo in autoimmune diseases using a mouse model of type II collagen-induced RA. Auditory brain stem response analysis demonstrated that the RA mouse models exhibited hearing loss, which is the primary symptom of AIED. In addition, our vestibulo-oculomotor reflex analysis, which is an excellent vestibular function test, accurately captured vertigo symptoms in the RA mouse models. Moreover, our results revealed that the cause of hearing loss and vestibular dysfunction was not endolymphatic hydrops, but rather structural destruction of the organ of Corti and the lateral semicircular canal ampulla due to an autoimmune reaction against type II collagen. Overall, we were able to establish a mouse model of AIED without endolymphatic hydrops. Our findings will help elucidate the mechanisms of hearing loss and vertigo associated with AIED and facilitate the development of new therapeutic methods., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier B.V. All rights reserved.)

Rheumatoid Arthritis (RA) is a chronic autoimmune inflammatory disease that affects about 0.1% to 2% of the population worldwide. Despite the development of several novel therapies, there is only limited benefit for many patients. Thus, there is room for new approaches to improve response to therapy, including designing better trials e.g., by identifying subpopulations that can benefit from specific classes of therapy and enabling reverse translation by analyzing completed clinical trials. We have developed an open-source, mechanistic multi-scale model of RA, which captures the interactions of key immune cells and mediators in an inflamed joint. The model consists of a treatment-naive Virtual Population (Vpop) that responds appropriately (i.e. as reported in clinical trials) to standard-of-care treatment options—Methotrexate (MTX) and Adalimumab (ADA, anti-TNF-α) and an MTX inadequate responder sub-population that responds appropriately to Tocilizumab (TCZ, anti-IL-6R) therapy. The clinical read-outs of interest are the American College of Rheumatology score (ACR score) and Disease Activity Score (DAS28-CRP), which is modeled to be dependent on the physiological variables in the model. Further, we have validated the Vpop by predicting the therapy response of TCZ on ADA Non-responders. This paper aims to share our approach, equations, and code to enable community evaluation and greater adoption of mechanistic models in drug development for autoimmune diseases. [ABSTRACT FROM AUTHOR]

Background: Secondary autoimmune disease (SAID) in the context of alemtuzumab treatment is one of the main safety concerns that may arise following administration in people with multiple sclerosis (pwMS). Contributing factors underlying this adverse event are not well understood. The purpose of this systematic review was to appraise the literature investigating the role of alemtuzumab in the development of SAID in pwMS following treatment and identify potential biomarkers/ risk factors that may be predictive of onset of this manifestation. Methods: Relevant publications were retrieved from PubMed, Embase, and Web of Science using a three-pronged search strategy containing the following keywords: "multiple sclerosis"; "alemtuzumab"; and "autoimmunity". Studies that fulfilled the specified eligibility criteria and investigated SAID development after alemtuzumab in pwMS were included in the final analysis. Results: 19 papers were included in the final review. Approximately, 47.92% of pwMS treated with alemtuzumab experienced SAID. A variety of biomarkers and risk factors were noted in the development of SAID, with a focus on immunological changes, including: increased homeostatic proliferation and T cell cycling, along with consistently elevated baseline serum IL-21 levels and thyroid autoantibodies. There was no significant association between known human leukocyte antigen (HLA) risk alleles, lymphocyte profile or dynamics and SAID development. Conclusions: While the mechanism underlying SAID following alemtuzumab is not fully understood, potential biomarkers and risk factors that may assist in elucidating mechanisms underlying this phenomenon have been documented in several independent studies. Following immunodepletion from alemtuzumab, an IL-21 driven increase in homeostatic proliferation and T cell cycling may disrupt tolerance mechanisms leading to an increase in the propensity toward alemtuzumab-induced autoimmunity. Further research is necessary to clarify the physiological changes after alemtuzumab therapy that trigger SAID in pwMS. [ABSTRACT FROM AUTHOR]

Immunity is a critical self-defense mechanism of the human body, wherein immune cells and immune molecules play a crucial role. Extracellular vesicles (EVs), derived from immune cells or other cells, play a significant role in tumors, autoimmune diseases and other immune-related disorders by serving as carriers and facilitating intercellular communication through the transfer of cargoes. Numerous studies have revealed that EVs can exacerbate disease development by modulating immune responses. Therefore, this paper focuses on the effects of EVs on the number, activity and function of different types of immune cells and the release of immune molecules (such as cytokines, antigens, antibodies, etc) in various diseases, as well as the roles of EVs associated with different types of immune cells in various diseases. We aim to provide a comprehensive review of the negative effects that EVs play in the immune system to provide more ideas and strategies for the management of clinical immune diseases. [ABSTRACT FROM AUTHOR]

Using nanostructured drug delivery systems has attracted increasing interest in immunotherapeutic approaches. The intrinsic immunomodulatory properties and versatility of nanoparticles used as carriers were consistently reported to augment treatment efficiency as nanoscaled materials increase drug accumulation at the desired site, enhance cell internalization, and improve therapeutic outcomes. Thus, numerous studies have exploited the potential use of nanostructured drug delivery vehicles in delivering different cargo as a promising alternative for treating conditions like cancer, autoimmune diseases, infectious diseases, and allergic and immune disorders. In this context, this paper presents nanostructured drug delivery systems as a solid basis for immunotherapeutic innovations, highlighting their advantages for improving treatment strategies, reviewing their clinical applications, and discussing existing challenges and ways to overcome them. [ABSTRACT FROM AUTHOR]

Objective: Alternative polyadenylation (APA) is a co-transcriptional process that leads to isoform diversity in the 3' ends of mRNAs. APA is known to occur during differentiation, and its dysregulation is observed in diseases like cancer and autoimmune disorders. It has been previously reported that differentiation of 3T3-L1 cells to adipocytes leads to an overall lengthening of mRNAs, but the proteins involved in this regulation have not been identified. The expression levels of subunits of the cleavage and polyadenylation (C/P) complex can regulate the choice of poly(A) site, which in turn can affect different cellular activities. In this paper, we studied the change in levels of C/P proteins during 3T3-L1 differentiation. Results: We observed that while the RNA expression of these proteins is unchanged during differentiation, the protein levels of some subunits do change, including a decrease in levels of CPSF73, the nuclease that cuts at the poly(A) site. However, overexpression of CPSF73 alone does not affect the efficiency and rate of differentiation. [ABSTRACT FROM AUTHOR]

This article is an editorial published in Frontiers in Psychiatry titled "Physical and medical conditions associated with autism." The editorial discusses the prevalence, causes, interventions, and long-term impacts of physical and medical conditions in autistic individuals. It highlights certain conditions such as sleep-wake disorders, epilepsy, and sensory impairments that are more common among autistic individuals. However, there are gaps in the literature regarding other conditions such as cardiovascular issues, immune dysregulation, genetic conditions, and constipation. The editorial also provides a summary of nine different papers included in the research topic, written by colleagues from various countries. These papers cover topics such as genetic and molecular mechanisms, immune dysregulation and inflammation, epidemiological and health profiles, treatment and strategies, and barriers to effective communication. The article emphasizes the importance of comprehensive medical assessments and individualized interventions for autistic individuals. [Extracted from the article]

This document is an editorial published in the journal Frontiers in Immunology. It discusses the role of myeloid-derived suppressor cells (MDSCs) in various health conditions and diseases, including cancer, autoimmunity, pregnancy, neonates, and aging. The editorial highlights the complexity of MDSCs and their potential as targets for immunotherapy. It also presents five research papers that provide insights into the multifaceted roles of MDSCs in oncogenesis, maternal-fetal interface, and aging, contributing to a better understanding of MDSCs biology and the development of more effective immunotherapeutic approaches. [Extracted from the article]

The 80+ existing autoimmune disorders (ADs) affect billions with little prevention or treatment options, except for temporary symptomatic management, leading to enormous human suffering and a monumental financial burden. The autoantibodies formed in most ADs have been identified, allowing the development of novel anti-idiotypic antibodies to mute the autoantibodies using vaccines. Nucleoside vaccines have been successfully tested as antigen-specific immunotherapies (ASI), with mRNA technology offering multi-epitope targeting to mute multiple autoantibodies. This paper proposes using mRNA technology to produce anti-idiotypic antibodies with broad effectiveness in preventing and treating them. This paper delves into the state-of-the-art mRNA design strategies used to develop novel ASIs by selecting appropriate T cell and B cell epitopes to generate anti-idiotypic antibodies. The low cost and fast development of mRNA vaccines make this technology the most affordable for the global control of ADs. [ABSTRACT FROM AUTHOR]

Abstract: Chimeric antigen receptor (CAR)-T cell therapy has achieved remarkable success in the treatment of hematological malignancies. Based on the immunomodulatory capability of CAR-T cells, efforts have turned toward exploring their potential in treating autoimmune diseases. Bibliometric analysis of 210 records from 128 academic journals published by 372 institutions in 40 countries/regions indicates a growing number of publications on CAR-T therapy for autoimmune diseases, covering a range of subtypes such as systemic lupus erythematosus, multiple sclerosis, among others. CAR-T therapy holds promise in mitigating several shortcomings, including the indiscriminate suppression of the immune system by traditional immunosuppressants, and non-sustaining therapeutic levels of monoclonal antibodies due to inherent pharmacokinetic constraints. By persisting and proliferating in vivo , CAR-T cells can offer a tailored and precise therapeutics. This paper reviewed preclinical experiments and clinical trials involving CAR-T and CAR-related therapies in various autoimmune diseases, incorporating innovations well-studied in the field of hematological tumors, aiming to explore a safe and effective therapeutic option for relapsed/refractory autoimmune diseases., (Copyright © 2024 The Chinese Medical Association, produced by Wolters Kluwer, Inc. under the CC-BY-NC-ND license.)

Autoimmune diseases can damage specific or multiple organs and tissues, influence the quality of life, and even cause disability and death. A 'disease in a dish' can be developed based on patients-derived induced pluripotent stem cells (iPSCs) and iPSCs-derived disease-relevant cell types to provide a platform for pathogenesis research, phenotypical assays, cell therapy, and drug discovery. With rapid progress in molecular biology research methods including genome-sequencing technology, epigenetic analysis, '-omics' analysis and organoid technology, large amount of data represents an opportunity to help in gaining an in-depth understanding of pathological mechanisms and developing novel therapeutic strategies for these diseases. This paper aimed to review the iPSCs-based research on phenotype confirmation, mechanism exploration, drug discovery, and cell therapy for autoimmune diseases, especially multiple sclerosis, inflammatory bowel disease, and type 1 diabetes using iPSCs and iPSCs-derived cells., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Ren, Jiang, Li and Zhang.)

Background and Purpose: The objective of this study is to evaluate the risk of secondary autoimmune diseases in multiple sclerosis (MS) patients treated with alemtuzumab (ALZ) through a meta-analysis., Methods: PubMed, Web of Science, OVID, EMBASE, and Cochrane central register of controlled trials were searched. Information and data were screened and extracted by 2 researchers. The obtained data were analyzed using the R software meta package. Quality assessment was conducted using the Newcastle-Ottawa Scale (NOS). The causes of heterogeneity were analyzed using subgroup analysis and sensitivity analysis. Publication bias was evaluated using funnel plots and Egger's test., Results: The search retrieved a total of 3530 papers from the databases. After screening, a total of 37 studies were included in the meta-analysis. The analysis results indicate that the pooled incidence rate of overall secondary autoimmune events (SAEs) in the included studies was 0.2824 [0.2348, 0.3300] (I²=94%, p<0.01). The overall incidence of autoimmune thyroid events (ATE) was 0.2257 [0.1810, 0.2703] (I²=94%, p<0.01). Among them, the rate of serious autoimmune thyroid events (SATE) was 0.0541 [0.0396, 0.0687] (I²=0%, p=0.44). The incidence rates of different thyroid events were as follows: Graves' disease (GD), 0.2266 [0.1632, 0.2900] (I²=83%, p<0.01); Hashimoto thyroiditis (HT), 0.0844 [0.0000, 0.2262] (I²=81%, p=0.02); Hashimoto thyroiditis with hypothyroidism (HTwH), 0.0499 [0.0058, 0.0940] (I²=37%, p=0.21); fluctuating thyroid dysfunction (FTD), 0.0219 [0.0015, 0.0424] (I²=0%, p=0.40); transient thyroiditis (TT), 0.0178 [0.0062, 0.0295] (I²=0%, p=0.94). The overall incidence of hematological events was 0.0431 [0.0274, 0.0621] (I²=70%, p<0.01). The incidence rates from high to low were as follows: lymphopenia, 0.0367 [0.0000, 0.0776] (I²=81%, p=0.02); Idiopathic thrombocytopenic purpura (ITP), 0.0258 [0.0199, 0.0323] (I²=25%, p=0.15); Hemolytic anemia (HA), 0.0177 [0.0081, 0.0391] (I²=29%, p=0.23); pancytopenia, 0.0136 [0.0000, 0.0314] (I²=0%, p=0.67); Neutropenia, 0.0081 [0.0000, 0.0183] (I²=0%, p=0.42). After excluding thyroid and hematological diseases, the combined incidence of other related SAEs was 0.0061 [0.0014, 0.0109] (I²=50%, p=0.02). The incidence of each disease ranked from highest to lowest as: skin psoriasis (SP), 0.0430 [0.0000, 0.0929] (I²=0%, p=0.57); alopecia areata (AA), 0.0159 [0.0024, 0.0372] (I²=19%, p=0.29); vitiligo, 0.0134 [0.0044, 0.0223] (I²=0%, p=0.81); inflammatory atrichia (IA), 0.0103 [0.0000, 0.0232] (I²=0%, p=0.43); chronic urticaria (CU), 0.0107 [0.0000, 0.0233] (I²=0%, p=0.60); and nephropathy, 0.0051 [0.0000, 0.0263] (I²=62%, p=0.02)., Conclusion: The occurrence of secondary autoimmune diseases in patients with MS treated with ALZ is noteworthy, particularly in the form of thyroid events and hematological events. Clinicians should monitor the overall condition of patients promptly for early management and avoid delayed diagnosis and treatment., Systematic Review Registration: inplasy.com/inplasy-2024-4-0048/, identifier INPLASY202440048., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Yang, Sun, Zhou, Zhang, Xu, Cao and Fan.)

Natural killer (NK) cells, a major component of the innate immune system, have prominent immunoregulatory, antitumor proliferation, and antiviral activities. NK cells act as a double-edged sword with therapeutic potential in neurological autoimmunity. Emerging evidence has identified NK cells are involved in the development and progression of neuroimmunological diseases such as multiple sclerosis, neuromyelitis optica spectrum disorders, autoimmune encephalitis, Guillain-Barré Syndrome, chronic inflammatory demyelinating polyneuropathy, myasthenia gravis, and idiopathic inflammatory myopathy. However, the regulatory mechanisms and functional roles of NK cells are highly variable in different clinical states of neuroimmunological diseases and need to be further determined. In this review, we summarize the evidence for the heterogenic involvement of NK cells in the above conditions. Further, we describe cutting-edge NK-cell-based immunotherapy for neuroimmunological diseases in preclinical and clinical development and highlight challenges that must be overcome to fully realize the therapeutic potential of NK cells., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

Background: Head and neck are a site of numerous pathologies with different aetiologies and presentations. Rare pathologies, although infrequent still do exist. Diagnostic dilemma in maxillofacial pathologies can be the most challenging situation. Dealing with uncertainty, although difficult, is a reality in surgical practice. Being thorough, attentive to details and clues, and maintaining an open mind are critical strategies in the approach to such a patient., Case Presentation: In our paper we are reporting a spectrum of 4 unusual variants of head and neck pathologies, whose age and sex were 52 years/ M, 37 years/F, 41 years/ F, 30 years/F respectively. All the patients were of Indian origin. The diagnosis ranged from autoimmune diseases to lymphatic cancer which posed a unique challenge both in the terms of diagnosis and management., Conclusion: A thorough systematic evaluation along with a multidisciplinary approach is mandatory in the diagnosis of unusual head and neck pathologies., (© 2024. The Author(s).)

Systemic lupus erythematosus (SLE) is a complex autoimmune disorder with a pathogenesis that remains incompletely understood, resulting in limited treatment options. MCC950, a highly specific NLRP3 inflammasome inhibitor, effectively suppresses the activation of NLRP3, thus reducing the production of caspase-1, the pro-inflammatory cytokines IL-1β and IL-18. This review highlights the pivotal role of NLRP3 inflammasome activation pathways in the pathogenesis of SLE and discusses the potential therapeutic application of MCC950 in SLE. Notably, it comprehensively elucidates the mechanism of MCC950 targeting the NLRP3 pathway in SLE treatment, outlining its potential role in regulating autophagy and necroptosis. The insights gained contribute to a deeper understanding of the value of MCC950 in SLE therapy, serving as a robust foundation for further research and potential clinical applications., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

RNA-based medicines are ideally suited for precise modulation of T cell phenotypes in anti-cancer immunity, in autoimmune diseases and for ex vivo modulation of T-cell-based therapies. Therefore, understanding productive siRNA uptake to T cells is of particular importance. Most studies used unmodified siRNAs or commercially available siRNAs with undisclosed chemical modification patterns to show functionality in T cells. Despite being an active field of research, robust siRNA delivery to T cells still represents a formidable challenge. Therefore, a systematic approach is needed to further optimize and understand productive siRNA uptake pathways to T cells. Here, we compared conjugate-mediated and nanoparticle-mediated delivery of siRNAs to T cells in the context of fully chemically modified RNA constructs. We showed that lipid-conjugate-mediated delivery outperforms lipid-nanoparticle-mediated and extracellular-vesicle-mediated delivery in activated T cells ex vivo. Yet, ex vivo manipulation of T cells without the need of activation is of great therapeutic interest for CAR-T, engineered TCR-T and allogeneic donor lymphocyte applications. We are first to report productive siRNA uptake into resting T cells using lipid-conjugate-mediated delivery. Interestingly, we observed strong dependence of silencing activity on lipid-conjugate-identity in resting T cells but not in activated T cells. This phenomenon is consistent with our early uptake kinetics data. Lipid-conjugates also enabled delivery of siRNA to all mononuclear immune cell types, including both lymphoid and myeloid lineages. These findings are expected to be broadly applicable for ex vivo modulation of immune cell therapies., Competing Interests: Declaration of Competing Interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests. Reka A Haraszti reports financial support was provided by German Cancer Aid. Reka A Haraszti reports financial support was provided by Faculty of Medicine, University of Tuebingen. If there are other authors, they declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

Background: Melkersson-Rosenthal syndrome (MRS) is a rare neuro-mucocutaneous disorder characterized by recurrent edema, facial palsies, and nerve dysfunctions often associated with the plicata tongue. Although the etiology of MRS is not well understood, there is growing evidence suggesting an autoimmune involvement. Case presentation: This paper presents a case report of a 25-year-old male with MRS as the initial symptom, followed by temporomandibular joint osteoarthritis (TMJ-OA). A comprehensive diagnosis and multidisciplinary treatment approach including surgery, local injections, and oral medication were implemented, resulting in a favorable prognosis. Conclusions: These findings support the hypothesis that MRS is a systemic granulomatous disease caused by autoimmunity, which may also influence the occurrence and development of TMJ-OA through immune-related mechanisms. This study emphasizes the significance of systemic immune regulation in the treatment of patients with MRS and TMJ-OA comorbid conditions. [ABSTRACT FROM AUTHOR]

Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease with a complex pathological mechanism involving autoimmune response, local inflammation and bone destruction. Metabolic pathways play an important role in immune-related diseases and their immune responses. The pathogenesis of rheumatoid arthritis may be related to its metabolic dysregulation. Moreover, histological techniques, including genomics, transcriptomics, proteomics and metabolomics, provide powerful tools for comprehensive analysis of molecular changes in biological systems. The present study explores the molecular and metabolic mechanisms of RA, emphasizing the central role of metabolic dysregulation in the RA disease process and highlighting the complexity of metabolic pathways, particularly metabolic remodeling in synovial tissues and its association with cytokine-mediated inflammation. This paper reveals the potential of histological techniques in identifying metabolically relevant therapeutic targets in RA; specifically, we summarize the genetic basis of RA and the dysregulated metabolic pathways, and explore their functional significance in the context of immune cell activation and differentiation. This study demonstrates the critical role of histological techniques in decoding the complex metabolic network of RA and discusses the integration of histological data with other types of biological data. [ABSTRACT FROM AUTHOR]

Immunosenescence, the gradual deterioration of immune function with age, holds profound implications for our understanding and management of multiple sclerosis (MS), a chronic autoimmune disease affecting the central nervous system. Traditionally diagnosed in young adults, advancements in disease-modifying therapies and increased life expectancy have led to a growing number of older individuals with MS. This demographic shift underscores the need for a deeper investigation into how age-related alterations in immune function shape the course of MS, influencing disease progression, treatment effectiveness, and overall patient outcomes. Age-related immunosenescence involves changes such as shifts in cytokine profiles, the accumulation of senescent immune cells, and compromised immune surveillance, collectively contributing to a state known as "inflammaging". In the context of MS, these immunological changes disturb the intricate balance between inflammatory and regulatory responses, thereby impacting mechanisms of central immune tolerance and peripheral regulation. This paper stands out by combining the most recent advancements in immunosenescence with both pathophysiological and treatment perspectives on multiple sclerosis, offering a cohesive and accessible discussion that bridges theory and practice, while also introducing novel insights into underexplored concepts such as therapy discontinuation and the latest senolytic, neuroprotective, and remyelination therapies. Enhancing our understanding of these complexities will guide tailored approaches to MS management, ultimately improving clinical outcomes for affected individuals. [ABSTRACT FROM AUTHOR]

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a debilitating disease with a broad overlap of symptomatology with Post-COVID Syndrome (PCS). Despite the severity of symptoms and various neurological, cardiovascular, microvascular, and skeletal muscular findings, no biomarkers have been identified. The Transient receptor potential melastatin 3 (TRPM3) channel, involved in pain transduction, thermosensation, transmitter and neuropeptide release, mechanoregulation, vasorelaxation, and immune defense, shows altered function in ME/CFS. Dysfunction of TRPM3 in natural killer (NK) cells, characterized by reduced calcium flux, has been observed in ME/CFS and PCS patients, suggesting a role in ineffective pathogen clearance and potential virus persistence and autoimmunity development. TRPM3 dysfunction in NK cells can be improved by naltrexone in vitro and ex vivo, which may explain the moderate clinical efficacy of low-dose naltrexone (LDN) treatment. We propose that TRPM3 dysfunction may have a broader involvement in ME/CFS pathophysiology, affecting other organs. This paper discusses TRPM3's expression in various organs and its potential impact on ME/CFS symptoms, with a focus on small nerve fibers and the brain, where TRPM3 is involved in presynaptic GABA release. [ABSTRACT FROM AUTHOR]

Autoimmune pancreatitis (AIP) is a unique form of chronic pancreatitis with a multifactorial pathogenesis. Historically, it has been classified as type 1 and type 2, according to its clinical and histological features. The diagnosis of AIP is challenging and relies on a combination of clinical, histopathologic, serologic, and imaging characteristics. In the available guidelines, the imaging hallmarks of AIP are based on cross-sectional imaging and cholangiopancreatography retrograde endoscopic findings. Endoscopic ultrasound (EUS) is generally used for pancreatic tissue acquisition to rule out pancreatic cancer and diagnose AIP with limited accuracy. Several papers reported the reliability of EUS for providing informative morphologic features of AIP. Nowadays, the improvement in the resolution of EUS conventional images and the development of new ancillary technologies have further increased the diagnostic yield of EUS: contrast-enhanced EUS and EUS elastography are non-invasive and real-time techniques that strongly support the diagnosis and management of pancreatic diseases. In this review article, we will present the role of conventional EUS and ancillary diagnostic techniques in the diagnosis of AIP to support clinicians and endosonographers in managing this condition. [ABSTRACT FROM AUTHOR]

Introduction: Systemic lupus erythematosus (SLE) is a chronic autoimmune disease. Mounting evidence suggests microbiota dysbiosis augment autoimmune response. This study aims to provide a systematic overview of this research field in SLE through a bibliometric analysis. Methods: We conducted a comprehensive search and retrieval of literature related to microbial researches in SLE from the Web of Science Core Collection (WOSCC) database. The retrieved articles were subjected to bibliometric analysis using VOSviewer and Bibliometricx to explore annual publication output, collaborative patterns, research hotspots, current research status, and emerging trends. Results: In this study, we conducted a comprehensive analysis of 218 research articles and 118 review articles. The quantity of publications rises annually, notably surging in 2015 and 2018. The United States and China emerged as the leading contributors in microbial research of SLE. Mashhad University of Medical Sciences had the highest publication outputs among the institutions. Frontiers in Immunology published the most papers. Luo XM and Margolles A were the most prolific and highly cited contributors among individual authors. Microbial research in SLE primarily focused on changes in microbial composition, particularly gut microbiota, as well as the mechanisms and practical applications in SLE. Recent trends emphasize "metabolites," "metabolomics," "fatty acids," "T cells," "lactobacillus," and "dietary supplementation," indicating a growing emphasis on microbial metabolism and interventions in SLE. Conclusion: This study provides a thorough analysis of the research landscape concerning microbiota in SLE. The microbial research in SLE mainly focused on three aspects: microbial dysbiosis, mechanism studies and translational studies (microbiota-based therapeutics). It identifies current research trends and focal points, offering valuable guidance for scholars in the field. [ABSTRACT FROM AUTHOR]