Prevalence Of Autoimmune Diseases Research Articles

Long-Term Outcomes and Quality of Life of High-Risk Neuroblastoma Patients Treated with a Multimodal Treatment Including Anti-GD2 Immunotherapy: A Retrospective Cohort Study.

The incorporation of anti-GD2 antibodies such as ch14.18/SP2/0 into the multimodal treatment of high-risk neuroblastoma (HR-NB) patients has improved their outcomes. As studies assessing the long-term outcomes, long-term sequelae, and health-related quality of life (HRQoL) of this treatment are limited, this retrospective analysis aimed to explore these. Between 1991 and 2002, 65 children received a multimodal treatment, including ch14.18/SP2/0, for primary HR-NB. All received chemotherapy according to the NB90/NB97 trial, 51 received high-dose chemotherapy, and all received ch14.18/SP2/0 treatment. We analyzed the long-term sequelae and HRQoL (EORTC QLQ-C30), and evaluated overall and event-free survival (OS/EFS). Twenty-five survivors were evaluated for HRQoL and long-term effects. All reported long-term sequelae, including ototoxicity in 16/25 (64%), cardiac toxicity in 6/25 (24%), and endocrine toxicity in 19/25 (76%) patients. Chronic diarrhea was reported in 20% of female patients. Seven patients developed autoimmune diseases. HRQoL scores were better across multiple scales than those of the matched German general population. Twenty-five-year OS and EFS were 50.8% (95% confidence interval: 31-55) and 43% (30.1-55.3), with 33 (50.8%) long-term survivors. Thirty-two patients died: 28 (43.1%) because of progression/relapse and 4 (6.2%) because of secondary neoplasms. Multimodal treatment, including ch14.18/SP2/0, can achieve long-term survival in HR-NB patients, with a substantial proportion of survivors reporting better HRQoL compared to the general population. All patients reported long-term side effects mostly attributable to chemotherapy and radiotherapy. The relatively high prevalence of autoimmune diseases and persistent diarrhea warrants additional longitudinal research on individuals treated with anti-GD2 antibodies.

Thoracic and Cardiovascular Imaging Manifestations of Lupus.

Systemic lupus erythematosus (SLE), commonly referred to as lupus, is a widely prevalent chronic autoimmune disease that can affect any organ system in the body. Although the pathogenesis of this disease is rather complex and poorly understood, ultimately there is an overproduction of multiple self-reactive antinuclear antibodies. These autoantibodies are one of the laboratory hallmarks of the diagnosis and disease activity of SLE. Lupus has a myriad of symptoms and imaging manifestations. Serositis, one of the most common manifestations of the disease, usually occurs with pleural or pericardial effusion with or without associated serosal inflammatory changes. The pulmonary manifestations are heterogeneous, with mostly acute (eg, diffuse alveolar hemorrhage, acute lupus pneumonitis) and some chronic (eg, fibrosing interstitial lung disease, shrinking lung syndrome) lung findings. Cardiac and vascular manifestations include myocarditis; coronary artery disease, including accelerated atherosclerosis; myocardial infarction; and spontaneous dissections, along with vasculitis, aneurysms, Libman-Sacks endocarditis, and arterial and venous thromboembolism. Although patient history and risk factor assessment have a vital role in diagnosing lupus, familiarity with the imaging manifestations aids radiologists in optimizing patient care, assessing for complications, and uncovering undiagnosed cases of lupus. This fact emphasizes the importance of recognizing the complex multisystem involvement of lupus seen at imaging. In this article, the authors review the thoracic and cardiovascular imaging manifestations of lupus. © RSNA, 2024.

Distinct clinical patterns in AQP4-IgG- positive NMOSD patients vs. Seronegative: Insights from a single-center study in Argentina.

Distinct clinical course patterns have been identified between AQP4-IgG-positive and AQP4-IgG-negative NMOSD patients. This study aimed to evaluate the differences between AQP4-IgG-seropositive and AQP4-IgG-seronegative NMOSD patients in a single centre in Argentina. We performed a retrospective cross-sectional study of 108 NMOSD patients in the city of Buenos Aires, Argentina. We selected 94 for analysis. 77 patients (82 %) were AQP4-IgG positive. In the AQP4-IgG positive group, the ratio of male to female was 1:10 vs. 1:1.2 in the seronegative group (p = 0.001). Relapses were observed in 76 out of 77 (99 %) AQP4-IgG positive patients versus 3 out of 17 (17.6 %) AQP4-IgG negative patients (p = 0.01). In the seropositive group, other autoimmune diseases were present in 34/77 patients (44 %) vs. 2/12 (12 %) in the seronegative patients, a statistically significant difference (p = 0.009). 81 % of the seropositive group had an early adulthood onset (EAO-NMOSD) compared to 35 % in the seronegative group. All AQP4+ patients positive received treatment with monoclonal antibodies. In AQP4-IgG- NMOSD patients the use of immunosuppressive treatment was more common. Female predominance, EAO-NMOSD, recurrence course and a high prevalence of autoimmune disease in AQP4-IgG-positive patients demonstrated a more pronounced autoimmunity profile.

COVID-19 is a trigger of autoimmune rheumatic diseases: a hypothesis tested over time.

We discuss the paper recently published in Rheumatology Internationa. This article reflects on the prevalence of autoimmune rheumatic diseases (ARD) during the COVID-19 pandemic (2020-2023) and compares the same with the pre-pandemic period (2016-2019). We assume that SARS-CoV-2 triggers ARD. This study concerns the 10million population of Greece, and this work convincingly confirms our hypothesis. Besides, four large cohort studies have demonstrated an increased incidence of autoimmune diseases after surviving COVID-19. Compared to the prepandemic period, all ARD increased, and RA growth in the index study reached a level of more than 20% during the pandemic. A similar trend was observed in our report covering four Central Asian republics, namely Kazakhstan, Kyrgyzstan, Uzbekistan, and Tajikistan. The alarming growth of ARDs due to the consequences of the pandemic can still be predicted for the coming years. Healthcare professionals worldwide should be aware of this hypothesis to plan their COVID-19, long COVID, and ARD diagnostic and therapeutic strategies. We agree with the authors of the index article that more resources and research studies are warranted to optimize the diagnosis and treatment of ARDs in this challenging time.

Crocin as a potential therapeutic agent for multiple sclerosis: insights from experimental autoimmune encephalomyelitis model in mice

Objective Multiple sclerosis (MS) is a prevalent autoimmune disorder characterized by neuroinflammation and demyelination in the central nervous system (CNS), leading to neurological dysfunction. Despite advances in treatment, there remains an unmet need for safe and effective therapies. Crocin, a bioactive constituent of saffron, has demonstrated anti-inflammatory and immunoregulatory properties in various disease models. This study investigates the therapeutic potential of Crocin in a murine model of MS, experimental autoimmune encephalomyelitis (EAE). Methods and results Female C57BL/6 mice were induced with EAE and treated with different doses of Crocin. Clinical severity, CNS pathology, T cell proliferation, cytokine production, and transcription factor expression were assessed. Crocin-treated mice showed reduced clinical severity, inflammation, and demyelination in the CNS compared to controls. Moreover, Crocin attenuated T cell proliferation and modulated cytokine production, promoting an anti-inflammatory cytokine profile while suppressing pro-inflammatory cytokines. Additionally, Crocin altered the expression of transcription factors associated with T cell differentiation, favoring regulatory T cell responses. Discussion These findings suggest that Crocin exerts therapeutic effects in EAE by modulating neuroinflammation and immune responses. Further studies are warranted to elucidate the mechanisms underlying Crocin’s immunomodulatory properties and its potential as a treatment for MS.

Genetic thrombophilia and antiphospholipid antibodies in women with early and late preeclampsia: a retrospective cohort study

Aim: to study a pattern of genetic and acquired thrombophilia in pregnant women with severe early-onset (eoPЕ) and severe late-onset PE (loPЕ) preeclampsia (PE).Materials and Methods. A retrospective cohort study was conducted from January 2022 to May 2024. A total of 109 pregnant women were examined: group 1 – 45 women with eoPЕ (< 34 weeks of pregnancy), group 2 – 24 women with loPЕ (≥ 34 weeks of pregnancy), group 3 (control) – 40 women with physiologically uncomplicated pregnancy. All pregnant women were examined for lupus anticoagulant (LA) and antiphospholipid antibodies (aPL). The screening test for aPL included the quantitation of IgG/IgM antibodies against cardiolipin, phosphatidylserine, phosphatidylinositol, phosphatidic acid, and β2-glycoprotein 1 in serum or plasma using an enzyme immunoassay. Genetic thrombophilia, homocysteine, and ADAMTS-13 metalloproteinase (a disintegrin and metalloproteinase with thrombospondin type 1 motif, member 13) levels were also determined.Results. Pregnant women with severe PE more often had genetic forms of thrombophilia (mutations in factor (F) V Leiden gene, prothrombin G20210A, and Thr165Met) and a deficiency of natural anticoagulants (antithrombin and protein S) compared to pregnant women in control group. Women in eoPE vs. loPE group were more often found to carry genetic polymorphisms in the plasminogen activator inhibitor-1 (PAI-1) and fibrinogen genes. Also, in the group of pregnant women with eoPE, the circulation of aPL, ADAMTS-13 inhibitor, and elevated homocysteine levels were more common. Pregnant women with loPE were older and more often suffered from hypertension, diabetes mellitus, and excess body weight. No significant differences between eoPЕ and loPЕ groups were found while comparing prevalence of autoimmune diseases, thrombosis in familial history, mutations in FV Leiden gene (heterozygous form), FII prothrombin gene G20210A (homozygous form), FII prothrombin gene Thr165Met (heterozygous form), antithrombin III deficiency, protein S deficiency.Conclusion. Precise causes underlying PE remain unknown, and we are still far from understanding all the molecular, immunological, genetic, and environmental mechanisms that lead to the various clinical manifestations of placental syndromes including PE. However, the study results suggest that the presence of thrombophilic disorders, especially in the fibrinolytic system, and aPL circulation contribute to eoPE pathophysiology or progression.

The climate emergency for rheumatologists: where do we stand?

Climate change and pollution are a major existential threat. Healthcare contributes a noteworthy 4-6% to the total carbon footprint and 5-7% of the total greenhouse gas (GHG) emissions. Environmental pollution and modern lifestyles are also contributing to the increased prevalence of autoimmune and lifestyle-related rheumatic disease. In this review, we assess both the effects of rheumatological practice on climate change and the potential impact of climate change on rheumatological diseases. Preliminary evidence suggests that climate change is linked with the inception or exacerbation of some of the autoimmune and inflammatoryrheumatic diseases (AIRDs) like rheumatoid arthritis, lupus, systemic sclerosis, and reactive arthritis. Furthermore, with rampant industrialization and pollution, emerging infections such as Dengue, Zika virus, and chikungunya have emerged as triggers of inflammatory arthritis. Strategies at different levels are proposed to mitigate the effect of the healthcare industry and the community on the environment. The rheumatology community can acknowledge and begin to address the challenges of climate change and health.

CAR T-cells in autoimmunity: game changer or stepping stone?

The advent of chimeric antigen receptor (CAR) T-cells has revolutionized the treatment landscape for hematologic malignancies, and emerging evidence suggests their potential in autoimmune diseases (AIDs). This article examines the early successes and future implications of B-cell-targeting CAR T-cell therapy in AIDs. Initial applications, particularly in refractory systemic lupus erythematosus (SLE), have demonstrated significant and durable clinical remissions, with accompanying evaluation of the immune system suggesting a so-called "reset" of innate inflammation and adaptive autoimmunity. This has generated widespread interest in expanding this therapeutic approach. CAR T-cells offer unique advantages over other treatment modalities, including very deep B-cell depletion and unique therapeutic activity within inflamed tissues and associated lymph structures. However, the field must address key concerns, including long-term toxicity, particularly the risk of secondary malignancies, and future accessibility given the higher prevalence of AIDs compared to malignancies. Technological advances in cell therapy, such as next-generation CAR T-cells, allogeneic off-the-shelf products and alternative cell types such as regulatory CAR T-cells, are being explored in AIDs to improve efficacy and safety. In addition, bispecific antibodies are emerging as potential alternatives or complements to CAR T-cells, potentially offering comparable efficacy without the need for complex logistics, lymphodepletion and the risk of insertional mutagenesis. As the field evolves, cellular therapists will play a critical role in the multidisciplinary teams managing these complex cases. The transformative potential of CAR T-cells in AIDs is undeniable, but careful consideration of safety, efficacy, and implementation is essential as this novel therapeutic approach moves forward.

Estimation of prevalence of autoimmune diseases in the United States using electronic health record data.

Previous epidemiologic studies of autoimmune diseases in the United States (US) have included a limited number of diseases or used meta-analyses that rely on different data collection methods and analyses for each disease. To estimate the prevalence of autoimmune diseases in the US, we used electronic health record data from six large medical systems in the US. We developed a software program using common methodology to compute the estimated prevalence of autoimmune diseases alone and in aggregate that can be readily used by other investigators to replicate or modify the analysis over time. Our findings indicate that over 15 million people, or 4.6% of the US population, have been diagnosed with at least one autoimmune disease from January 1, 2011, to June 1, 2022, and 34% of those are diagnosed with more than one autoimmune disease. As expected, females (63% of those with autoimmune disease) were almost twice as likely as males to be diagnosed with an autoimmune disease. We identified the top 20 autoimmune diseases based on prevalence and according to sex and age. Thus, we provide, for the first time, a large-scale prevalence estimate of autoimmune disease in the US by sex and age. Autoimmune Registry Inc., the National Heart Lung and Blood Institute, the National Center for Advancing Translational Sciences, the Intramural Research Program of the National Institute of Environmental Health Sciences.

Elevated thyroid-stimulating hormone levels, independent of Hashimoto's thyroiditis, increase thyroid cancer risk: Insights from genetic and clinical evidence.

Hashimoto's thyroiditis (HT) is a prevalent autoimmune disorder and thyroid cancer (TC) is the most prevalent endocrine malignancy. Recent debates have focused on whether HT increases the risk of developing TC. This study combined Mendelian randomization (MR) and observational methods to investigate the potential causal relationship between HT and TC risk. First, we performed two-sample MR and multivariable MR (MVMR) analysis using the genome-wide association studies (GWAS) data from multiple databases, including European and East Asian populations, to estimate the effect of HT and thyroid-stimulating hormone (TSH) levels on TC risk. Second, we conducted an observational study using data from the National Health and Nutrition Examination Survey (NHANES) database and evaluated the association between HT, TSH, and TC prevalence through logistic regression model and restricted cubic spline model. Our MR findings revealed no significant association between HT and TC risk in both populations. However, elevated TSH levels significantly increased TC and papillary thyroid carcinoma (PTC) risk, while lower TSH levels were associated with reduced TC risk. Further MVMR analysis and an observational study confirmed this. Additionally, our observational study also indicated no significant relationship between HT and TC prevalence and abnormal TSH levels correlated with higher TC risk. HT was not a TC risk factor, but high TSH levels increased TC risk. Controlling TSH within normal ranges through thyroid hormone replacement was recommended to reduce TC risk in HT patients with elevated TSH levels, even those without symptoms.

Dietary factors and rheumatoid arthritis: new perspectives from a Mendelian randomisation analysis.

Rheumatoid arthritis (RA) is a prevalent autoimmune disease, and there is growing evidence suggesting a potential correlation between dietary factors and the pathogenesis of this condition. In order to investigate the causal relationship between diet and RA, we conducted a two-sample Mendelian randomisation (MR) analysis to examine the causal associations between twenty-two dietary factors and RA. Summary data from genome-wide association studies (GWAS) of RA were obtained from large GWAS meta-analyses. GWAS summary data for twenty-two dietary factors were obtained from UK Biobank. Random-effects inverse variance weighted was used as the primary method for assessing causality, and analyses of heterogeneity and horizontal pleiotropy were performed to ensure the accuracy of the results. Research indicates a negative genetic causal relationship between cereal intake (OR = 0·64, 95 % CI: 0·41, 0·99, P = 0·048) and oily fish intake (OR = 0·70, 95 % CI: 0·52, 0·95, P = 0·020) with the risk of RA. Other dietary factors were not causally related to RA. Sensitivity analysis shows that our results are reliable. This study provides genetic evidence suggesting that cereal intake and oily fish intake are protective factors for RA, indicating that RA patients and individuals at high risk should make appropriate dietary adjustments.

Mindfulness Therapy for Autoimmune Diseases in Indonesia: Mechanisms, Applications, and Challenges

Mindfulness therapy, a psychological approach emphasizing awareness of the present experience without judgment, has gained attention as a potential intervention for improving the quality of life of patients with autoimmune diseases in Indonesia. With the increasing prevalence of autoimmune diseases and their associated physical and psychological symptoms, mindfulness therapy is highly relevant. This review explored the mechanisms of action, case studies, challenges, and recommendations for implementing mindfulness therapy in Indonesia. Mindfulness has been shown to modulate brain activity associated with emotional processing, reduce inflammation, improve pain management, enhance social relationships, and improve sleep quality. Case studies in Indonesia have demonstrated the effectiveness of mindfulness therapy in patients with rheumatoid arthritis and lupus, with participants reporting significant improvements in their physical and mental symptoms. However, challenges such as insufficient understanding among medical personnel, societal stigma, limited availability of programs, cultural factors, and lack of comprehensive research need to be addressed. Recommendations include enhanced education and training for medical personnel, public awareness initiatives, the development of culturally appropriate programs, improved accessibility, and further research on the effectiveness of mindfulness therapy in Indonesia. By addressing these challenges and implementing recommendations, mindfulness therapy can be effectively integrated into the Indonesian healthcare system to improve patient's quality of life with autoimmune diseases.

Decreased prevalence and altered clinical phenotype of systemic sclerosis and other autoimmune connective tissue diseases in type 1 and type 2 diabetes: A cross-sectional observational study.

Evidence has demonstrated that autoimmune diseases tend to coexist at a higher rate than expected, reflecting a common pathogenic pathway. In this study, we investigate the co-occurrence of systemic sclerosis, systemic lupus erythematosus, and Sjogren syndrome in patients with type 1 and type 2 diabetes mellitus. Our data were obtained using the 2019 Healthcare Cost and Utilization Project, and International Classification of Diseases, 10th Revision diagnosis codes were used to identify patients with systemic sclerosis, systemic lupus erythematosus, lupus nephritis, and Sjogren syndrome, as well as patients with type 1 and type 2 diabetes. We utilized Statistical Analysis System 9.4 for all analyses and included designated weight values to produce nationally representative estimates. The prevalence of systemic sclerosis among patients with type 1 diabetes mellitus and type 2 diabetes mellitus was significantly lower than that for the non-diabetes mellitus control group (0.0007% vs 0.09%, p-value = 0.0064 and 0.01% vs 0.07%, p-value < 0.0001), respectively. Similarly, there was a significant decrease in the prevalence of systemic sclerosis with lung involvement in patients with type 1 and type 2 diabetes mellitus, with a statically significant difference in type 2 diabetes mellitus versus nondiabetic group (0.001% vs 0.006%, p-value < 0.0001). We noted a similar pattern regarding the prevalence of systemic lupus erythematosus and lupus nephritis in patients with type 1 and 2 diabetes. Similarly, there was a significant decrease in the prevalence of Sjogren syndrome in patients with type 1 diabetes and type 2 diabetes. The collected data demonstrates an inverse relation between some autoimmune connective tissue diseases and diabetes. This suggests that these diseases and diabetes mellitus may have different immune pathogenesis. There was also a significantly lower incidence of organ complications such as lupus nephritis and systemic sclerosis lung disease among patients with diabetes, suggesting that diabetes and treatment of diabetes may alter the clinical expression of these disorders.

The use of hyaluronic acid fillers in patients with autoimmune endocrinopathies; in particular, women with Hashimoto's disease - hints for aesthetic doctors.

The increase of the incidence of autoimmune diseases and, at the same time, a significant surge in the number of regenerative/anti-aging medicine treatments carried out, raises the need to systematise the current knowledge on the safety of the use of hyaluronic acid fillers in patients with autoimmune diseases and to frame management guidelines for aesthetic doctors. One of the most prevalent autoimmune diseases is chronic lymphocytic thyroiditis, so-called Hashimoto's disease, which affects one in every 5-10 women who visit a regenerative medicine doctor. Women in the perimenopausal and menopausal period, aged 40-54 years, were the single largest target group for aesthetic treatments. At the same time, Hashimoto's disease, similarly to other autoimmune disorders, constitutes a contraindication to most treatments with hyaluronic acid fillers and biostimulators. Due to the dysfunction of the immune system in this group of patients, there is a higher risk of adverse side effects, especially those of immunological nature. Based on the available literature, the incidence of adverse reactions after the use of hyaluronic acid-based fillers amounts to 0.01-1% and is undoubtedly underestimated. The most typical one is recurrent oedema and granulomas. The following paper reviews the existing literature on the safety of hyaluronic acid fillers in patients with autoimmune endocrinopathies.

Lactoferrin alleviates oxidative stress and endoplasmic reticulum stress induced by autoimmune thyroiditis by modulating the mTOR pathway in the thyroid.

Autoimmune thyroiditis (AITD) is a prevalent autoimmune disorder characterized by the immune system's attack on thyroid tissue, potentially leading to thyroid dysfunction, with a current lack of effective treatment modalities. Lactoferrin, a crucial functional dietary component obtainable from food sources, primarily exists in mammalian milk. We aim to investigate whether dietary supplementation with lactoferrin can protect the thyroid in Experimental Autoimmune Thyroiditis (EAT) rats. Our study reveals significantly elevated levels of oxidative stress (OS) and endoplasmic reticulum stress (ERS) in the AITD. Lactoferrin markedly reduces OS and infiltration of inflammatory cells in the thyroid tissue of EAT rats. Furthermore, lactoferrin inhibits ERS levels in the thyroid of EAT rats and alleviates cellular apoptosis. In vivo and in vitro experiments elucidate that its protective effect is primarily achieved through the inhibition of mTOR signaling pathway activation. In summary, lactoferrin, a nutrient readily obtainable from food sources, appears to be effective in mitigating thyroid damage in AITD.

Assessment of Immunological, Skeletal, and Thyroid Function Abnormalities in Paediatric Morphoea

Abstract Background: Morphoea is a sclerosing disorder of skin and subcutaneous tissue. Paediatric morphoea shows increased prevalence of various auto-immune diseases, bone deformities, and systemic abnormalities. There is paucity of studies on various immunological, skeletal, and thyroid function abnormalities in paediatric morphoea. Aims and Objectives: To describe immunological, skeletal, and thyroid function abnormalities present in paediatric morphoea patients. Materials and Methods: This cross-sectional study was conducted from January 2021 to March 2023 in the Dermatology outpatient department in a tertiary care hospital. All paediatric morphoea patients were included in this study. All were subjected to detailed history, clinical examination, and investigations including complete blood count, serum IgE, anti-nuclear antibody, thyroid function tests, anti-thyroid peroxidase antibodies, and radiological investigations. Results: A total of 42 children were recruited, out of which 61.90% were females and 38.09% were males. The majority were in the age group of 4–8 years. The most common type of morphoea was encoup de sabre. Anaemia was present in 14.28% patients. Serum IgE levels were raised in 33.33% patients. Thyroid stimulating hormone was raised in 11.9% patients. 33.33% had raised anti-thyroid peroxidase levels. Anti-nuclear antibody titres and rheumatoid factor were raised in 7.14% and 4.76% patients, respectively. Magnetic resonance imaging brain revealed abnormalities in three patients as hyper-intensities in subcortical white matter. Conclusion: Morphoea in children can be associated with varied immunological, osteoarticular, and neurological abnormalities. This study highlights the multi-system involvement in morphoea and the need for larger data and well-designed therapeutic trials for generating evidence-based treatment of this potentially disfiguring disease.

Prevalence of comorbid autoimmune diseases and antibodies in newly diagnosed multiple sclerosis patients

BackgroundDiagnosing multiple sclerosis (MS) is challenging due to diverse symptoms and the absence of specific biomarkers. Concurrent autoimmune diseases (AID) or non-specific antibodies further complicate diagnosis, progression monitoring, and management. Data on AID prevalence in MS patients are sparse. This study aims to identify concurrent AIDs alongside MS.MethodsIn this retrospective single-center study, we analyzed patient records at our university hospital from 2010 to 2017, focusing on cases suspected of inflammatory demyelinating disease. The 2017 McDonald criteria were applied. Additionally, we measured neurofilament light (NfL) levels from available CSF samples in our biobank.ResultsWe identified a total of 315 patients, of whom 66% were women. In total, 13.7% of all patients had concurrent AID, while 20.3% had isolated antibody findings without AID. The most common AID was autoimmune thyroiditis (8.9%), followed by chronic inflammatory skin diseases (1.6%), arthritis (1%), type 1 diabetes (1%), Sjögren’s syndrome (0.6%), and inflammatory bowel diseases (0.6%). Cardiolipin antibodies were the most frequent isolated antibody finding (8.6%). Our data showed that, from the perspective of the initial demyelinating event, neither comorbid AID nor isolated antibodies significantly influenced relapses or MS progression over a median follow-up of 9 months. Standard CSF parameters and NfL levels were similar between the groups at the time of MS diagnosis.ConclusionOur study shows that AIDs, particularly autoimmune thyroiditis, frequently occur at the onset of MS. The proportion of AIDs commonly treated with immunomodulatory therapy in our cohort was similar to that observed in the general population. Comorbid AID did not affect NfL levels, indicating similar disease activity. Future research should explore new AID emergence during the course of MS, especially considering the increased incidence of rheumatic diseases later in life.

Prevalence of Autoimmune Thyroiditis Among Children with Type 1 Diabetes

A single-stage cross-sectional study was conducted on the basis of the National Center for Maternal Health in the Kyrgyz Republic, children aged 0 to 18 years were examined. To study the prevalence of autoimmune thyroid disease with type 1 diabetes mellitus to improve the compensation of carbohydrate metabolism in children and adolescents with type 1 diabetes. Autoimmune thyroiditis often accompanies and interferes with type 1 diabetes mellitus in children and adolescents. Thyroid dysfunction in children with type 1 diabetes mellitus can negatively affect various areas of metabolic control. This study included 60 children with type 1 diabetes mellitus and autoimmune thyroiditis, 24 of them girls (40.0%), 36 boys (60%). The average value of ±SD for their age at the time of examination was 11.6±4.1 years, ranging from 1 to 17 years. Of the children with type 1 diabetes mellitus who tested positive for antibodies to thyroid peroxidase, 30 children (50%) had obvious hypothyroidism. Of the thirty children with normal TSH levels, 4 children (13.3%) showed signs of subclinical hypothyroidism, while 26 children (86.7%) had euthyroidism.

Dual-targeted halofuginone hydrobromide nanocomplexes for promotion of macrophage repolarization and apoptosis of rheumatoid arthritis fibroblast-like synoviocytes in adjuvant-induced arthritis in rats

Rheumatoid arthritis (RA) is a prevalent autoimmune disease characterized by chronic inflammation and excessive proliferation of the synovium. Currently, treatment options focus on either reducing inflammation or inhibiting synovial hyperplasia. However, these modalities are unsatisfactory in achieving the desired therapeutic outcomes. Halofuginone hydrobromide (HF), an herbal active ingredient, has demonstrated pharmacological effects of both anti-inflammation and inhibition of synovial hyperplasia proliferation. However, HF’s medical efficacy is limited due to its poor water solubility, short half-life, and non-target toxicity. In the current study, by using the advantages of nanotechnology, we presented a novel dual-targeted nanocomplex, termed HA-M@P@HF NPs, which consisted of a hyaluronic acid (HA)-modified hybrid membrane (M)-camouflaged poly lactic-co-glycolic acid (PLGA) nanosystem for HF delivery. These nanocomplexes not only overcame the limitations of HF but also achieved simultaneous targeting of inflammatory macrophages and human fibroblast-like synoviocytes-rheumatoid arthritis (HFLS-RA). In vivo experiments demonstrated that these nanocomplexes effectively suppressed immune-mediated inflammation and synovial hyperplasia, safeguarding against bone destruction in rats with adjuvant-induced arthritis (AIA). Remarkable anti-arthritic effects of these nanocomplexes were accomplished through promoting repolarization of M1-to-M2 macrophages and apoptosis of HFLS-RA, thereby offering a promising therapeutic strategy for RA.

CCR5 mediates rheumatoid arthritis progression by promoting the activation and proliferation of non-classical Th1 cells.

Rheumatoid arthritis (RA) is a prevalent autoimmune disease characterized by immune dysegulation, including an immune imbalance due to abnormal activation of non-classical Th1 cells (CD161+ Th1). This study investigated the effects of CCR5 on the activation and proliferation of CD161+ Th1 and their pathogenicity in patients with RA. The study was conducted on 53 patients with RA and 32 age- and sex-matched healthy controls (HC). The cell phenotype was assessed by flow cytometry and the cytokine levels in the supernatant were detected by ELISA. We demonstrate a marked increase in CD161+ Th1 cells in the synovial fluid of RA patients. These cells exhibit a hyperactivated and hyperproliferative state alongside elevated CCR5 expression. Furthermore, the levels of CD161+ Th1 cells, CD25, and CCR5 in RA synovial fluid show a positive correlation with the disease activity. Additionally, our study reveals that CCR5 facilitates the activation, proliferation, and cytokine production of CD161+ Th1 cells through the pZAP70/NFAT signaling pathway. These findings contribute to a deeper understanding of RA pathogenesis and uncover a novel mechanism that regulates non-classical CD161+ Th1 responses in RA, which may provide a potential therapeutic target.