Prevalence Of Autoimmune Diseases Research Articles

The Mechanism of "Treating Different Diseases with the Same Treatment" by Qiangji Jianpi Decoction in Ankylosing Spondylitis Combined with Inflammatory Bowel Disease: A Comprehensive Analysis of Multiple Methods.

Ankylosing spondylitis (AS) and inflammatory bowel disease (IBD) are prevalent autoimmune disorders that often co-occur, posing significant treatment challenges. This investigation adopts a multidisciplinary strategy, integrating bioinformatics, network pharmacology, molecular docking, and Mendelian randomization, to elucidate the relationship between AS and IBD and to investigate the potential mechanisms of traditional Chinese medicine formulations, represented by Qiangji Jianpi (QJJP) decoction, in treating these comorbid conditions. We utilized databases to pinpoint common targets among AS, IBD, and QJJP decoction's active compounds through intersection analysis. Through Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses, we mapped a network in Cytoscape, isolating critical targets. Molecular docking with AutoDock validated the affinity between targets and compounds. ROC analysis and dataset validation assessed diagnostic performance, while Gene Set Enrichment Analysis (GSEA) offered pathway insights. Mendelian randomization explored the AS-IBD causal relationship. Screening identified 105 targets for QJJP decoction, 414 for AS, and 2420 for IBD, with 85 overlapping. These targets predominantly participate in organismal responses and DNA transcription factor binding, with a significant cellular presence in the endoplasmic reticulum and vesicle lumen. Molecular docking, facilitated by Cytoscape, confirmed IL1A, IFNG, TGFB1, and EDN1 as critical targets, with IFNG demonstrating diagnostic potential through GEO dataset validation. The integration of GSEA with network pharmacology highlighted the therapeutic significance of the relaxin, osteoclast differentiation, HIF-1, and AGE-RAGE signaling pathways in QJJP decoction's action. Mendelian randomization analysis indicated a positive causal relationship between IBD and AS, pinpointing rs2193041 as a key SNP influencing IFNG. Based on the principle of "treating different diseases with the same method" in traditional Chinese medicine theory, we explored the intricate mechanisms through which QJJP decoction addresses AS and IBD comorbidity. Our research spotlighted the pivotal role of the IFNG gene. IFNG emerges not only as a key therapeutic target but also assumes significance as a potential diagnostic biomarker through its genetic underpinnings. This investigation establishes a solid base for subsequent experimental inquiries. Our findings introduce novel approaches for incorporating traditional Chinese medicine into the treatment of AS-IBD comorbidity, setting the stage for groundbreaking research directions.

Prevalence of Autoimmune Diseases Among Patients With Psoriasis: A Single Tertiary Center Experience.

Background Psoriasis is a common chronicinflammatory skin disease with an autoimmune etiology. Psoriasis has been presumed to be associated with several autoimmune diseases. We sought to determine the prevalence of autoimmune diseases in patients with psoriasis in a large referral tertiary care center. Methods This is a retrospective and cross-sectional chart review of patients with confirmed psoriasis diagnoses in the dermatology clinic of King Abdulaziz Medical City, Riyadh, Saudi Arabia. The electronic charts of patients were individually reviewed for autoimmune diseases such as hypothyroidism, hyperthyroidism, alopecia areata, vitiligo, atopic dermatitis, and inflammatory bowel diseases like Crohn's disease and celiac diseases. Results A total of 839 cases were included, 56.4% of whom were females. Most patients were between 31 and 50 years old (37.1%). The most common autoimmune disease was hypothyroidism (6.8%), seen more in females. The second most common autoimmune disease was alopecia areata (3.6%), followed by atopic dermatitis (2.9%). Rheumatoid arthritis,systemic lupus erythematosus, and inflammatory bowel diseases were uncommon in our cohort. Conclusion In this single-center retrospective cohort of patients with psoriasis, hypothyroidismand alopecia areata were the most commonly encountered autoimmune diseases. Larger, multi-center studies are needed to evaluate the prevalence of autoimmune diseases among patients with psoriasis.

The relationship of peripheral blood lncRNA-PVT1 and miR-146a levels with Th17/Treg cytokines in patients with Hashimoto's thyroiditis and their clinical significance.

Hashimoto's thyroiditis (HT) is a prevalent autoimmune disease. We investigated the relationship of peripheral blood long noncoding RNA-plasmacytoma variant translocation 1 (lncRNA-PVT1) and microRNA (miR)-146a levels with Th17/Treg-related cytokines in HT patients and their clinical significance. Correlations of PVT1 and miR-146a with Th17/Treg-related cytokines were analyzed, and its clinical value in diagnosing HT was assessed. Results showed reduced lncRNA-PVT1 and interleukin (IL)-10 levels and increased miR-146a and IL-17 levels in HT patients. lncRNA-PVT1 negatively interrelated with miR-146a, IL-17, IL-23 and IL-6, and positively interrelated with IL-10; miR-146a positively correlated with IL-17, IL-23 and IL-6, but negatively correlated with IL-10 in HT patients. The area under the curve (AUC) of lncRNA-PVT1and miR-146a levels for diagnosing HT were 0.822 and 0.844, respectively (sensitivity 88.73% and 86.62%, specificity 67.02% and 69.15%, cut-off values 0.76 and 2.73), with their combined detections yielding a higher AUC. Patients with poorly expressed lncRNA-PVT1 and highly expressed miR-146a had elevated HT incidence. lncRNA-PVT1 and miR-146a levels were also found to be an independent influencing factor for HT occurrence. Our findings suggest that HT patients have low peripheral blood lncRNA-PVT1expression and high miR-146a expression. lncRNA-PVT1and miR-146a level changes were correlated with Th17/Treg cytokine imbalance and could be a potential diagnostic tool and independent influencing factor for HT.

Research Progress of Natural Active Substances with Immunosuppressive Activity.

The increasing prevalence of autoimmune diseases globally has prompted extensive research and the development of immunosuppressants. Currently, immunosuppressive drugs such as cyclosporine, rapamycin, and tacrolimus have been utilized in clinical practice. However, long-term use of these drugs may lead to a series of adverse effects. Therefore, there is an urgent need to explore novel drug candidates for treating autoimmune diseases. This review aims to find potential candidate molecules for natural immunosuppressive compounds derived from plants, animals, and fungi over the past decade. These compounds include terpenoids, alkaloids, phenolic compounds, flavonoids, and others. Among them, compounds 49, 151, 173, 200, 204, and 247 have excellent activity; their IC50 were less than 1 μM. A total of 109 compounds have good immunosuppressive activity, with IC50 ranging from 1 to 10 μM. These active compounds have high medicinal potential. The names, sources, structures, immunosuppressive activity, and the structure-activity relationship were summarized and analyzed.

The prevalence of serious autoimmune diseases is increased in women with premature ovarian insufficiency in Finland - A population-based study

The prevalence of serious autoimmune diseases is increased in women with premature ovarian insufficiency in Finland - A population-based study

Development of a novel long-acting injectable, IVL4002 for modulation of multiple sclerosis: Pharmacokinetics and efficacy studies in an experimental autoimmune encephalomyelitis mouse model

Abstract Multiple sclerosis (MS), a prevalent autoimmune disease and lacking a well-defined etiology and cures, drove the development of diverse disease-modifying therapies (DMTs). Despite the efficacy of DMTs and immunosuppressants, challenges persist, including adverse effects and varying response rates. A promising approach involves the utilization of a novel drug delivery system (DDS) for controlled drug release. Herein, we introduce a novel long-acting injectable (LAI) designed for MS modulation, IVL4002, developed using IVL-DrugFluidics™ manufacturing platform. IVL4002 comprises monodisperse microspheres encapsulating an FDA-approved drug which was discovered by drug repurposing. The selected drug has been utilized in the clinic for a non-MS CNS indication with a favorable safety profile and has also been used in autoimmune diseases off-label for decades. As shown in the preclinical pharmacokinetics studies, IVL4002 maintains drug levels within the target range over 4 weeks without a burst release. Combined with the advanced DDS, the drug was repurposed for MS management, of which the efficacy was shown in experimental autoimmune encephalomyelitis mice by reducing the pro-inflammatory cytokine release. In conclusion, our physicochemical and pharmacological studies underscored the potential of IVL4002 to be used as a 1-month LAI for MS management. Positive results have led to the approval of a Phase 1 clinical trial and it is expected to begin in the second-half of 2024.

The Immunomodulatory Effects and Mechanism of Wogonin for the Treatment of Multiple Sclerosis in a Murine Experimental Autoimmune Encephalomyelitis Model

Abstract Multiple sclerosis (MS) stands out as the most prevalent inflammatory autoimmune disease affecting the central nervous system (CNS). The primary driver of MS involves myelin-specific autoreactive T cells that infiltrate the CNS, initiating attacks on myelinated axons and triggering neuroinflammatory responses. Wogonin, a flavonoid, exhibits pharmacologic properties, including neuroprotective, anticancer, antiviral, anti-inflammatory, and anti-oxyradical effects. Our study demonstrates that wogonin significantly suppresses TLR-dependent DC activation, migration, and the expression of adhesion molecules in LPS-stimulated bone marrow-derived dendritic cells (BMDCs). In the experimental autoimmune encephalomyelitis (EAE) model, preventive treatment with wogonin led to reduced lymphocyte infiltration, prevented demyelination in the CNS, and consequently mitigated disease symptoms. Moreover, wogonin suppressed the release of neuroinflammatory cytokines by activated microglial cells, Th1 cells, Th2 cells, and Th17 cells in vitro and exerted therapeutic effects on attenuating the disease severity in the early disease onset stage and late disease progression stage. Our study suggests that wogonin treatment may not only prevent the onset of MS by inhibiting DC activation and migration but also potentially ameliorate the progression of MS by reducing neuroinflammation. This opens avenues for the development of new approaches in the therapy of autoimmune diseases.

Celiac Disease and Autoimmune Diseases in a Pediatric Population in Morocco: A Cross-Sectional Study.

Celiac disease (CD) is defined as an autoimmune disease (AD) caused by gluten ingestion in genetically sensitive individuals. Several publications have demonstrated the increased risk of AD in patients with CD, both adults and children, which requires systematic research. Our study aimed to determine the prevalence of AD in 60 patients diagnosed with CD and to highlight risk factors that may contribute to the emergence of AD. We collected medical data from all CD patients under 16 years of age who also had AD. Our study was conducted in the Gastroenterology-Hepatology and Pediatric Nutrition Unit of the Pediatrics Department of the Mohamed VI Hospital and University Center in Oujda, Morocco, during a seven-year period between January 2017 and January 2024. We studied 60 patients with CD in our study. Eight patients (13%) had an associated AD. Their average age was eight years, with extremes varying between two and 15 years. AD was diagnosed before CD in six cases (75%), in parallel with CD in one patient (12.5%), while in only one case, it was diagnosed after CD (12.5%).All our patients had a single AD associated with CD. These ADs were mainly type 1 diabetes in seven cases and autoimmune thyroiditis in only one case. All our patients followed a gluten-free diet in addition to specific treatment for associated AD. Nevertheless, despite regular medical follow-up and targeted dietary advice for the management of CD and associated AD, three patients encountered difficulties in following the recommended diet. Younger patients with CD have an increased risk of hypothyroidism and insulin-dependent diabetes. These data necessitate improved surveillance to discover these illnesses as early as possible in order to optimize management and reduce related consequences.

Exploring cGAS-STING Pathway in Sjögren’s Disease: Driver of IFN production and Potential Therapeutic Target

Abstract Sjögren's Disease (SjD) is a prevalent autoimmune disorder characterized by dysfunctional lacrimal and salivary glands (SG) and lacks an effective therapy. Despite unknown pathogenic mechanisms, elevated interferon (IFN) expression is observed in SjD patients. Recent findings indicate activation of the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway in systemic lupus, prompting investigation into its role in SjD. We hypothesize cGAS-STING pathway activation in SjD contributing IFN dysregulation and symptoms. Bulk and single-cell RNA sequencing of SjD SG shows elevated IFN-related genes in epithelial and inflammatory cells. Investigation of the affected human SG by flow cytometry confirms upregulated phosphorylation status of cGAS-STING proteins in epithelial and immune cells; and epithelial cGAS-STING pathway activation directly correlates with the level of immune cell infiltration. Treatment of patient’s SG and peripheral blood mononuclear cells (PBMC) with a STING antagonist ex vivo reduces phosphorylated protein levels without cytotoxicity. These findings support our hypothesis that targeting the cGAS-STING pathway holds promise for mitigating salivary gland inflammation in SjD, preventing chronic inflammation's secondary effects and resulting tissue destruction.

A role of DRAK2 in regulatory T cell (Treg) survival and T cell metabolic reprogramming

Abstract Multiple Sclerosis (MS), one of the prevalent autoimmune disorders causing damage to the brain and spinal cord, requires safer therapeutics since current therapies rely on general immunosuppression, rendering patients susceptible to infection. Prior studies revealed that DAP kinase-related apoptosis-inducing protein kinase 2 (DRAK2) KO mice exhibit resistance to EAE, a mouse model for MS. DRAK2 deficiency also induced an overall reduction in T cell proliferation but an increase in proportion of regulatory T cells (Tregs) upon in vitro stimulation, potentially due to metabolic shift in T cells. To investigate the impact of DRAK2 deficiency on the expansion of different T cell subsets and how it reshapes T cell metabolism, WT and DRAK2-/- mice were used to quantify different T cell subsets and inspect significant alterations in mitochondrial metabolism. Results demonstrated decreased effector T cells and lipid contents in DRAK2-/- mouse T cells upon stimulation. A DRAK2 deficiency displayed an increase in mitochondrial membrane potential using JC-1 and TMRE staining of mouse T cells. RNA sequencing of T cells in WT and DRAK2-/- mice revealed that the absence of DRAK2 promotes the expression of TRIM family proteins which are closely associated with cGAS-STING DNA sensing pathway presumably caused by mtDNA. Altogether, these findings support the hypothesis that DRAK2 serves as a key metabolic regulator in T cells, heightening its potential as a new therapeutic target for MS.

Graves’ disease and the risk of five autoimmune diseases: A Mendelian randomization and colocalization study

BackgroundEpidemiological studies have consistently demonstrated a high prevalence of concurrent autoimmune diseases in individuals with Graves' disease (GD). ObjectiveThe objective of this study is to establish a causal association between GD and autoimmune diseases. MethodsWe employed a two-sample Mendelian randomization (MR) to infer a causal association between GD and five autoimmune diseases, namely rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), Crohn's disease (CD), ulcerative colitis (UC), and amyotrophic lateral sclerosis (ALS), in the East Asian and European population. Genetic correlations were explored through linkage disequilibrium score regression analysis (LDSC). Finally, colocalization analyses were performed to investigate possible genetic foundations. ResultsBidirectional MR analysis indicated that genetically predicted GD increased the risk of RA (Odds Ratio (OR): 1.34, 95 % Confidence Interval (CI): 1.21 to 1.47, P < 0.001) and SLE (OR: 1.21, 95%CI: 1.08 to 1.35, P < 0.001) in the East Asian population. In contrast, we found that genetically predicted RA (OR: 1.14, 95%CI: 1.05 to 1.24, P = 0.002) and SLE (OR: 1.10, 95%CI: 1.03 to 1.17, P = 0.003) were associated with a higher risk of GD. The results have been partially validated in European cohorts. Colocalization analysis suggested the potential existence of shared causal variants between GD and other autoimmune diseases. In particular, gene ARID5B may play an important role in the incidence of autoimmune diseases. ConclusionThis study has confirmed that GD was associated with RA and SLE and found a possible key gene ARID5B. It may be necessary to strengthen detection to prevent the occurrence of comorbidities in clinical practice.

Comorbidities, mortality and metabolic profile in individuals with primary biliary cholangitis-A Phenome-Wide-Association-Study.

Primary biliary cholangitis (PBC) is a chronic, immune-mediated liver disease that can lead to fibrosis and cirrhosis. In this cohort study, we aimed to investigate morbidity and mortality in conjunction with metabolomic changes of PBC in a UK population-based cohort. 454 participants with PBC and 908 propensity score (age, sex, BMI, ethnicity) matched controls without liver disease were included in the study. A subset of participants with PBC and controls were analysed for their metabolomic profile. Further, PBC-associated comorbidities were investigated by PheWAS analysis. Lastly, we assessed causes of death in individuals with PBC using a Fine and Grey competing-risks regression model. Compared to the control group, various pathways associated with the metabolism of amino acids, lipids, and liver biochemistry were significantly enriched in individuals with PBC. We found reduced levels of S-HDL-cholesterol and Glycoprotein Acetyls in individuals with PBC as well as an association with diseases of the circulatory system. Notably, PBC individuals had a higher prevalence of digestive diseases, autoimmune diseases, cardiovascular diseases, anaemias, mental disorders, and urinary tract infections compared to the control group. Strikingly, the overall mortality was almost three times higher in the PBC group compared to the control group, with diseases of the digestive system accounting for a significant elevation of the death rate. A subsequent analysis, enhanced by propensity score matching that included the APRI score, demonstrated that the observed morbidity could not be exclusively attributed to advanced hepatic disease. Our study provides a detailed perspective on the morbidity of individuals with PBC. The exploration of potential effects of disease state on morbidity suggest that early detection and early treatment of PBC could enhance patient prognosis and prevent the onset of comorbid diseases. Finally, the metabolomic alterations could represent a link between the pathophysiological processes underlying PBC development, progression, and associated morbidity.

Prevalence of autoimmune thyroiditis among children with autoimmune hepatitis.

Autoimmune hepatitis (AIH) is an organ specific autoimmune disease, which can manifest at any age of life. there is a high prevalence of extrahepatic autoimmune diseases in patients with AIH. Autoimmune thyroid diseases (ATDs) are the most frequent extrahepatic autoimmune disorders among patients with AIH. Aim of work is to detect the frequency of ATDs among Egyptian children with AIH. This research is a cross-sectional study conducted on 58 children with AIH aged ≤ 18years. All patients were tested for free triiodothyronine (FT3), free tetraiodothyronine (FT4), thyroid stimulating hormone (TSH), anti-thyroid peroxidase (anti-TPO) and antithyroglobulin (anti-TG). Thyroid ultrasound (US) and thyroid scan were performed for patients with abnormal thyroid profile, borderline values, positive anti-TPO or anti-TG. The mean ± standard deviation (SD) for the age of the patients was 11.3 ± 4.5years. Out of 58 patients of AIH, 28 patients (48.3%) had associated other autoimmune diseases. Autoimmune thyroiditis was the most common associated autoimmune disease being present in 10 patients (17.2%). The thyroid status of AIT patients showed that 6 patients (60%) were euthyroid, 3 patients (30%) had subclinical hypothyroidism and only one patient (10%) was hyperthyroid. Autoimmune hepatitis in Egyptian children is commonly associated with other autoimmune diseases. Autoimmune thyroiditis is the most common to be associated with AIH in pediatric patients. As it is not usually clinically manifesting, regular screening for AIT in children with AIH is mandatory.

Identifying serum metabolite biomarkers for autoimmune diseases: a two-sample mendelian randomization and meta-analysis.

Extensive evidence suggests a link between alterations in serum metabolite composition and various autoimmune diseases (ADs). Nevertheless, the causal relationship underlying these correlations and their potential utility as dependable biomarkers for early AD detection remain uncertain. The objective of this study was to employ a two-sample Mendelian randomization (MR) approach to ascertain the causal relationship between serum metabolites and ADs. Additionally, a meta-analysis incorporating data from diverse samples was conducted to enhance the validation of this causal effect. A two-sample MR analysis was performed to investigate the association between 486 human serum metabolites and six prevalent autoimmune diseases: systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), inflammatory bowel disease (IBD), dermatomyositis (DM), type 1 diabetes (T1D), and celiac disease (CeD). The inverse variance weighted (IVW) model was employed as the primary analytical technique for the two-sample MR analysis, aiming to identify blood metabolites linked with autoimmune diseases. Independent outcome samples were utilized for further validation of significant blood metabolites. Additional sensitivity analyses, including heterogeneity test, horizontal pleiotropy test, and retention rate analysis, were conducted. The results from these analyses were subsequently meta-integrated. Finally, metabolic pathway analysis was performed using the KEGG and Small Molecule Pathway Databases (SMPD). Following the discovery and replication phases, eight metabolites were identified as causally associated with various autoimmune diseases, encompassing five lipid metabolism types: 1-oleoylglycerophosphoethanolamine, 1-arachidonoylglycerophosphoethanolamine, 1-myristoylglycerophosphocholine, arachidonate (20:4 n6), and glycerol. The meta-analysis indicated that three out of these eight metabolites exhibited a protective effect, while the remaining five were designated as pathogenic factors. The robustness of these associations was further confirmed through sensitivity analysis. Moreover, an investigation into metabolic pathways revealed a significant correlation between galactose metabolism and autoimmune diseases. This study revealed a causal relationship between lipid metabolites and ADs, providing novel insights into the mechanism of AD development mediated by serum metabolites and possible biomarkers for early diagnosis.

Prevalences of Other Non-Thyroid Autoimmune Diseases and Factor Associated with Their Presence in Ocular Myasthenia Gravis.

To report the prevalences of other non-thyroid autoimmune diseases and identify factors associated with their presence in ocular myasthenia gravis (OMG) subjects. A total of 208 subjects with OMG diagnosis were included. Demographic data, clinical characteristics, the ice-pack test, the acetylcholine receptor (AChR) antibody test, electrophysiology tests (single-fiber electromyography and repetitive nerve stimulation), the presence of thymoma, generalized myasthenia gravis conversion, and the presence of other non-thyroid autoimmune diseases (defined as the presence of at least one other non-thyroid autoimmune disease) were retrospectively reviewed. Factors associated with the presence of other non-thyroid autoimmune diseases were analyzed by univariate and multivariate logistic regression. Of the total 208 subjects, 21 (10.10%) exhibited the presence of other non-thyroid autoimmune diseases (19 subjects (9.14%) and 2 subjects (0.96%) had one and two other non-thyroid autoimmune diseases, respectively), and systemic lupus erythematosus (SLE) was diagnosed in 9 subjects, followed by Sjogren's syndrome (7 subjects), rheumatoid arthritis (6 subjects), and ankylosing spondylitis (1 subject). Therefore, the prevalences of SLE, Sjogren's syndrome, rheumatoid arthritis, and ankylosing spondylitis in OMG subjects were estimated to be 4.33% (95% confidence interval (CI): 2.29-8.02%), 3.37% (95% CI: 1.64-6.79%), 2.88% (95% CI: 1.33-6.14%), and 0.48% (95% CI: 0.08-2.67%), respectively. Positivity of the AChR antibody was the only significant factor associated with the presence of other non-thyroid autoimmune diseases (odds ratio 4.10, 95% CI: 1.11-15.21, p = 0.035). The presence of other non-thyroid autoimmune diseases was found in approximately 10% of OMG patients, with SLE displaying the highest prevalence. We recommend screening and monitoring for other non-thyroid autoimmune diseases in OMG patients, particularly those with positivity of the AChR antibody.

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.

Prevalence of autoimmune diseases in patients with sickle cell disease: a single center retrospective analysis.

Not available.

Comparative Analysis of the Two Innovative Vaccines

Multiple sclerosis (MS), one of the most prevalent autoimmune diseases, poses a significant challenge for therapeutic advancements. Among these, antigen-specific therapies (ASTs) utilizing therapeutic vaccines have emerged as highly promising. Designed to induce antigen-specific tolerance without compromising the overall immune system, these vaccines offer a glimmer of hope for MS patients, despite many still being in the preclinical trial phase. This research provides an elaborate comparison of two distinct vaccine types: m1Ψ mRNA vaccines and ROS-scavenging CeNP MSN vaccines. As AST vaccines targeting MS, they exhibit notable similarities across various facets, ranging from superficial aspects such as the models employed to evaluate therapeutic effects to deeper considerations like their anti-inflammatory characteristics and key mechanistic factors. Beneath these similarities, significant differences are identified and analyzed within this article. Additionally, the advantages, disadvantages, and noteworthy features of each vaccine are thoroughly compared, accompanied by corresponding suggestions for improvement. Through this comparative analysis of the two innovative vaccines, the paper aims to enhance readers' comprehension of MS treatments. By offering humble insights, it aspires to make a positive impact on related research, ultimately contributing to the advancement of MS therapeutic approaches.

Comparison of Low-Dose Interleukin 2 Therapy in Conjunction With Standard Therapy in Patients With Systemic Lupus Erythematosus vs Rheumatoid Arthritis: A Systematic Review.

This systematic review aims to compare the efficacy and safety of a novel immunotherapy with low-dose interleukin 2 (IL2) across two of the most prevalent autoimmune diseases i.e. systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). Contemporary therapeutic practices have not been able to achieve complete remission from these autoimmune disorders. In contrast, low-dose IL2has shown promise in achieving this therapeutic goal via inducing self-tolerance in patients with autoimmune diseases; however, due to variable irregularities among autoimmune processes of variable diseases, the benefit of low-dose IL2 could not be determined among different autoimmune diseases. Therefore, we conducted a study to compare low-dose IL2 therapy effects on SLE and RA. We systematically screened four databases: PubMed, Medical Literature Analysis and Retrieval System Online (MEDLINE), PubMed Central (PMC), and Google Scholar. Inclusion and exclusion criteria were implemented. Quality appraisal of studies chosen for the review was done using the Cochrane Risk-of-Bias (RoB) assessment tool for randomized controlled trials, and the Newcastle-Ottawa Scale (NOS) and JBI critical appraisal tool for non-randomized clinical trials. Information was gathered from seven articles: three randomized controlled trials and four non-randomized clinical trials. Our review concluded that low-dose IL2 therapy in conjunction with respective standard therapies for SLE and RA has a higher efficacy and safety profile as compared to standard therapy alone and the therapeutic effects were comparable in both SLE and RA patients treated with low-dose IL2; however, this novel intervention does not seem to have a significant corrective effect on the biomarkers of RA as it does for SLE biomarkers.

A Review of Some the Physiological Effects of Methotrexate on Rheumatoid Arthritis

Rheumatoid arthritis is one of the most prevalent autoimmune diseases at the present time, and it affects both sexes and is characterized by the incidence of women more than men about 1:3. Arthritis causes many negative effects in the various body systems, represented by the lymphatic, respiratory, muscular and blood systems, in addition to its effect on the heart, blood vessels and kidneys. Cytokines have an important role in stimulating the occurrence of rheumatoid arthritis, and these cytokines (IL-1, TNF-α, IL-8) attract inflammatory cells to the synovial membrane due to the erosion of bones and joints. Amethopterin, 4-amino 4-deoxy-N10-methylpteroyl-glutamic acid is a folate antagonist) developed more than 50 years ago in combination with several antifolate therapies used to fight malignant tumors. This review study Further elucidation of the mechanism of methotrexate to treat RA in the patients Methotrexate remains the mainstay of RA treatment and it important to identify the patients in whom the drug is effective and those in which toxicity may be an issue. Genetic and biomarkers may help to stratify patients and possibly shed light on the mechanism for efficacy and for toxicity of methotrexate for RA.