[Autoimmune hearing loss and a chance of its development in children: literature review and own observations]. / Autoimmunnaya tugoukhost' i veroyatnost' ee formirovaniya v detskom vozraste: obzor literatury i sobstvennye nablyudeniya.

Autoimmune sensorineural hearing loss (AiSNHL) is an uncommon auditory disorder characterized by rapidly progressive bilateral hearing loss and a positive clinical response to treatment with corticosteroids and cytostatics. The prevalence of the disease in the adult population is less than 1% among all cases of subacute and permanent sensorineural hearing loss (precise data are unknown), it is even rarer in children. AiSNHL can be primary (isolated, organ-specific) or secondary (manifestation of another systemic autoimmune disease). The pathogenesis of AiSNHL is based on the proliferation of autoaggressive T cells and the pathological production of autoantibodies to the protein structures of the inner ear, which leads to damage to various parts of the cochlea (possibly also to the retrocochlear parts of the auditory system), less frequently to the vestibular labyrinth. Pathologically, the disease is most often represented by cochlear vasculitis with degeneration of the vascular stria, damage to hair cells and spiral ganglion cells, and endolymphatic hydrops. In 50% of cases, the result of autoimmune inflammation may be fibrosis and/or ossification of the cochlea. The most characteristic symptoms of AiSNHL at any age are episodes of sudden progression of hearing loss, fluctuations of hearing thresholds, and bilateral, often asymmetric impairments. The article presents contemporary ideas of the clinical and audiological manifestations of AiSNHL, the possibilities of diagnosing and treating the disease, and highlights the current approaches to (re)habilitation. Along with literature data, two own clinical cases of an extremely rare pediatric AiSNHL are given.

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

Autoimmunity refers to the phenomenon that the body's immune system produces antibodies or sensitized lymphocytes to its own tissues to cause an immune response. Immune disorders caused by autoimmunity can mediate autoimmune diseases. Autoimmune diseases have complicated pathogenesis due to the many types of cells involved, and the mechanism is still unclear. The emergence of single-cell research technology can solve the problem that ordinary transcriptome technology cannot be accurate to cell type. It provides unbiased results through independent analysis of cells in tissues and provides more mRNA information for identifying cell subpopulations, which provides a novel approach to study disruption of immune tolerance and disturbance of pro-inflammatory pathways on a cellular basis. It may fundamentally change the understanding of molecular pathways in the pathogenesis of autoimmune diseases and develop targeted drugs. Single-cell transcriptome sequencing (scRNA-seq) has been widely applied in autoimmune diseases, which provides a powerful tool for demonstrating the cellular heterogeneity of tissues involved in various immune inflammations, identifying pathogenic cell populations, and revealing the mechanism of disease occurrence and development. This review describes the principles of scRNA-seq, introduces common sequencing platforms and practical procedures, and focuses on the progress of scRNA-seq in 41 autoimmune diseases, which include 9 systemic autoimmune diseases and autoinflammatory diseases (rheumatoid arthritis, systemic lupus erythematosus, etc.) and 32 organ-specific autoimmune diseases (5 Skin diseases, 3 Nervous system diseases, 4 Eye diseases, 2 Respiratory system diseases, 2 Circulatory system diseases, 6 Liver, Gallbladder and Pancreas diseases, 2 Gastrointestinal system diseases, 3 Muscle, Bones and joint diseases, 3 Urinary system diseases, 2 Reproductive system diseases). This review also prospects the molecular mechanism targets of autoimmune diseases from the multi-molecular level and multi-dimensional analysis combined with single-cell multi-omics sequencing technology (such as scRNA-seq, Single cell ATAC-seq and single cell immune group library sequencing), which provides a reference for further exploring the pathogenesis and marker screening of autoimmune diseases and autoimmune inflammatory diseases in the future.

Pesticide use and risk of systemic autoimmune diseases in the Agricultural Health Study.

BACKGROUND: Systemic lupus erythematosus (SLE) risk has been associated with pesticide use, but evidence on specific pesticides or other agricultural exposures is lacking. We investigated history of pesticide use and risk of SLE and a related disease, Sjögren's syndrome (SS), in the Agricultural Health Study. METHODS: The study sample (N = 54,419, 52% male, enrolled in 1993-1997) included licensed pesticide applicators from North Carolina and Iowa and spouses who completed any of the follow-up questionnaires (1999-2003, 2005-2010, 2013-2015). Self-reported cases were confirmed by medical records or medication use (total: 107 incident SLE or SS, 79% female). We examined ever use of 31 pesticides and farm tasks and exposures reported at enrollment in association with SLE/SS, using Cox regression to estimate hazard ratios (HR) and 95% confidence intervals (CI), with age as the timescale and adjusting for gender, state, and correlated pesticides. RESULTS: In older participants (>62 years), SLE/SS was associated with ever use of the herbicide metribuzin (HR 5.33; 95%CI 2.19, 12.96) and applying pesticides 20+ days per year (2.97; 1.20, 7.33). Inverse associations were seen for petroleum oil/distillates (0.39; 0.18, 0.87) and the insecticide carbaryl (0.56; 0.36, 0.87). SLE/SS was inversely associated with having a childhood farm residence (0.59; 0.39, 0.91), but was not associated with other farm tasks/exposures (except welding, HR 2.65; 95%CI 0.96, 7.35). CONCLUSIONS: These findings suggest that some agricultural pesticides may be associated with higher or lower risk of SLE/SS. However, the overall risk associated with farming appears complex, involving other factors and childhood exposures.

Immunomodulatory effects of curcumin in systemic autoimmune diseases.

Systemic autoimmune diseases like rheumatoid arthritis, multiple sclerosis, and systemic lupus erythematosus represent various autoimmune conditions identified by immune system dysregulation. The activation of immune cells, auto-antigen outbreak, inflammation, and multi-organ impairment is observed in these disorders. The immune system is an essential complex network of cells and chemical mediators which defends the organism's integrity against foreign microorganisms, and its precise operation and stability are compulsory to avoid a wide range of medical complications. Curcumin is a phenolic ingredient extracted from turmeric and belongs to the Zingiberaceae, or ginger family. Curcumin has multiple functions, such as inhibiting inflammation, oxidative stress, tumor cell proliferation, cell death, and infection. Nevertheless, the immunomodulatory influence of curcumin on immunological reactions/processes remains mostly unknown. In the present narrative review, we sought to provide current information concerning the preclinical and clinical uses of curcumin in systemic autoimmune diseases.

The Interplay between Autonomic Nervous System and Inflammation across Systemic Autoimmune Diseases.

The autonomic nervous system (ANS) and the immune system are deeply interrelated. The ANS regulates both innate and adaptive immunity through the sympathetic and parasympathetic branches, and an imbalance in this system can determine an altered inflammatory response as typically observed in chronic conditions such as systemic autoimmune diseases. Rheumatoid arthritis, systemic lupus erythematosus, and systemic sclerosis all show a dysfunction of the ANS that is mutually related to the increase in inflammation and cardiovascular risk. Moreover, an interaction between ANS and the gut microbiota has direct effects on inflammation homeostasis. Recently vagal stimulation techniques have emerged as an unprecedented possibility to reduce ANS dysfunction, especially in chronic diseases characterized by pain and a decreased quality of life as well as in chronic inflammation.

COVID-19 vaccine literacy in patients with systemic autoimmune diseases.

COVID-19 related infodemic is a threat to the successful COVID-19 vaccination campaigns. This might be especially apparent for patients with autoimmune diseases since there is no data available about the balance between benefits and risks of the newly developed COVID-19 vaccines in this population. We aim (i) to evaluate vaccine literacy skills in a population of patients with systemic autoimmune diseases, (ii) to examine the potential associations between vaccine literacy skills and sociodemographic characteristics and (iii) to analyze the relationships between attitudes, perceptions and beliefs about current vaccinations and vaccine literacy skills and sociodemographic characteristics. A cross-sectional study was conducted among 319 patients with systemic autoimmune diseases (92% females; 49.5% of patients in the 31-50 years age category). The vaccine literacy levels were determined using the Health Literacy about Vaccination in adulthood in Italian (HLVa-IT). Sociodemographic characteristics including gender, age, country and area of residence, civil status, socioeconomic status, educational attainment and occupational status were evaluated. The mean vaccine literacy functional and interactive-critical scores were 2.59 ± 0.74 and 3.07 ± 0.60, respectively. The vaccine literacy interactive-critical score was higher in females than in males (p = 0.048). Interactive-critical scores were associated with the area of residence, civil status and socioeconomic status, with the highest score in urban area of ≥ 100.000 inhabitants (p = 0.045), in widow patients (p = 0.023) and in patients with high socioeconomic status (p = 0.018). Significant differences were observed between the different education levels, for both the functional and the interactive-critical scores (p = 0.002 and p < 0.001, respectively), the highest score was observed in patients who completed a university degree. The level of vaccine literacy for functional and interactive-critical scales were medium. Area of residence, civil status and socioeconomic status represented determinants of vaccine literacy interactive-critical scale. Educational attainment also contributes to vaccine literacy functional scale. Insight into these factors is required to ensure an optimal vaccine literacy level in patients with autoimmune diseases. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s12144-022-02713-y.

Thymus variants on imaging in patients with rheumatoid arthritis-clinical and immunological significance.

OBJECTIVES: We sought to clarify the presence of radiographic thymus variants using a scoring system, and their association with clinical and immunological features in RA patients. METHODS: A total of 387 RA patients were randomly selected from all patients visiting our department who underwent chest CT scanning, with exclusion of patients with thymoma or thymic cyst, or age < 30 years. Thymus size and attenuation score in axial CT images were quantitatively interpreted and assessed. Associations between immunophenotype data and clinical and serological features were analysed in a subset of patients. RESULTS: Thymic enlargement was found in 76 (19.6%) patients, and a thymus attenuation score ≥ 2 was found in 50 (12.9%) patients. The score was significantly associated with antibodies to ACPA positivity. Thymic enlargement was significantly associated with the proportions of CD4+ effector memory T cells. CONCLUSION: Radiographic thymus variants were frequently observed in RA patients and may reflect an abnormal immune response involved in the pathogenesis of RA.

[Antinuclear antibodies : Practical diagnostic recommendations for dermatologists]. / Antinukleäre Antikörper : Praktische Empfehlungen zur Diagnostik durch den Dermatologen.

Antinuclear antibodies (ANA) are a common diagnostic finding in patients with systemic autoimmune diseases. In patients with typical clinical symptoms, the determination of ANA is of both diagnostic and prognostic importance. However, if ANA were determined due to unspecific symptoms, the interpretation of ANA findings can be problematic. In these cases, misjudgements with severe consequences for the patients are possible. Many systemic autoimmune diseases have prominent early skin involvement and the dermatologist can be the first physician that such a patient sees. Therefore, knowledge of ANA diagnostics is important for dermatologists. Basic principles of autoantibody diagnostics, guidance for the interpretation of laboratory results and new developments are discussed in this overview.

Metabolic Disturbances in Urinary and Plasma Samples from Seven Different Systemic Autoimmune Diseases Detected by HPLC-ESI-QTOF-MS.

Systemic autoimmune diseases (SADs) are characterized by dysfunctioning of the immune system, which causes damage in several tissues and organs. Among these pathologies are systemic lupus erythematosus (SLE), systemic sclerosis or scleroderma, Sjögren's syndrome, rheumatoid arthritis, primary antiphospholipid syndrome (PAPS), mixed connective tissue disease (MCTD), and undifferentiated connective tissue disease (UCTD). Early diagnosis is difficult due to similarity in symptoms, signs, and clinical test results. Hence, our aim was to search for differentiating metabolites of these diseases in plasma and urine samples. We performed metabolomic profiling by liquid chromatography-mass spectrometry (LC-MS) of samples from 228 SADs patients and 55 healthy volunteers. Multivariate PLS models were applied to investigate classification accuracies and identify metabolites differentiating SADs and healthy controls. Furthermore, we specifically investigated UCTD against the other SADs. PLS models were able to classify most SADs vs healthy controls (area under the roc curve (AUC) > 0.7), with the exception of MCTD and PAPS. Differentiating metabolites consisted predominantly of unsaturated fatty acids, acylglycines, acylcarnitines, and amino acids. In accordance with the difficulties in defining UCTD, the UCTD metabolome did not differentiate well from the other SADs. However, most UCTD cases were classified as SLE, suggesting that metabolomics may provide a tool to reassess UCTD diagnosis into other conditions for more well-informed therapeutic strategies.

Antiphospholipid autoantibody detection is important in all patients with systemic autoimmune diseases.

Antiphospholipid (aPL) autoantibodies are uncommon in systemic autoimmune diseases (SADs). However, the European PRECISESADS study provides the opportunity to better characterize this rare association. The study was composed of 1818 patients with SADs including 453 with systemic lupus erythematosus (SLE), 359 with rheumatoid arthritis (RA), 385 with systemic sclerosis (SSc), 367 with Sjögren's syndrome (SjS), 94 with mixed connective tissue disease (MCTD), and 160 with undifferentiated connective tissue disease (UCTD). Assays used for aPL determination include the lupus anticoagulant (LAC) analysis using the dilute Russell's viper venom time (dRVVT) assay plus anti-cardiolipin (aCL) and anti-aß2GPI autoantibodies of IgG and IgM isotype. Information regarding clinical and biological characteristics of SAD patients was available. Among SAD patients, the prevalence of aPL differs significantly between two groups: SLE (57.6%) and non-SLE SADs (13.7%, p < 10-4). Next, association between aPL plus thrombosis and miscarriage were observed in both SLE and non-SLE patients. Thrombosis was best predicted in SLE patients by dRVVT (OR = 6.1; IC95:3.5-10.3) and miscarriage by aCL±ß2GPI IgG (OR = 2.5; IC95:1.2-5.2); while in non-SLE SADs the best predictors were aCL±ß2GPI IgG for thrombosis (OR = 6.6; IC95:2.4-18.4) and aCL±ß2GPI IgM for miscarriage (OR = 2.9; IC95:1.2-6.8). In the case of multiple positivity of aPL, the risk for thrombosis and miscarriage was increased. Central nervous system involvement characterized the SLE patients, in contrast to pulmonary and skin fibrosis, valve lesions, hypertension, elevated creatinemia, C4 fraction reduction, platelet reduction and inflammation that characterized the non-SLE SAD patients. Anti-PL determination remains important in SADs patients and should not be restricted to only SLE patients.

Extremely high levels of multiple cytokines in the cord blood of neonates born to mothers with systemic autoimmune diseases.

Most infants born to mothers with autoimmune diseases are thought to be entirely healthy. However, the immunological conditions have not been examined thoroughly. Fourteen neonates born to mothers with systemic autoimmune diseases, namely systemic lupus erythematosus, mixed connective tissue disease, Sjögren's syndrome, rheumatoid arthritis, and systemic sclerosis, were included. Serum concentrations of 17 cytokines from the infants' umbilical artery (UA) and vein (UV) and from the mothers' peripheral blood were investigated by a bead array system. Cytokine expression in the placenta was investigated by immunohistochemical staining. The disease was controlled in all mothers, and none had chorioamnionitis. Hypercytokinemia was found in 11 neonates irrespective of their mothers' autoimmune diseases. In six neonates, serum cytokines were at extremely high levels. Four neonates were born by cesarean section because of a non-reassuring fetal status (NRFS) of unknown cause were all included in the hypercytokinemia group. However, all the subjects were discharged without any complications. The cytokine levels were almost the same between UA and UV, but the mothers' blood samples did not show elevation of serum cytokines. There were no differences in the expression of cytokines in the placenta among three patients with different serum cytokines levels. Hypercytokinemia frequently occurred and a cytokine storm state sometimes developed in neonates born to mothers with systemic autoimmune diseases. Growth restriction and NRFS may be related to hypercytokinemia in utero. It is plausible that the high level of cytokines in cord blood originate in neither the mother nor the placenta but in fetal immune tissues. It is important to investigate the immunological mechanisms, prevalence, and long-term influence of hypercytokinemia in a large sample size of neonates and mothers with systemic autoimmune diseases.

Role of microRNAs in the Development of Cardiovascular Disease in Systemic Autoimmune Disorders.

Rheumatoid Arthritis (RA), Systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS) are the systemic autoimmune diseases (SADs) most associated with an increased risk of developing cardiovascular (CV) events. Cardiovascular disease (CVD) in SADs results from a complex interaction between traditional CV-risk factors, immune deregulation and disease activity. Oxidative stress, dyslipidemia, endothelial dysfunction, inflammatory/prothrombotic mediators (cytokines/chemokines, adipokines, proteases, adhesion-receptors, NETosis-derived-products, and intracellular-signaling molecules) have been implicated in these vascular pathologies. Genetic and genomic analyses further allowed the identification of signatures explaining the pro-atherothrombotic profiles in RA, SLE and APS. However, gene modulation has left significant gaps in our understanding of CV co-morbidities in SADs. MicroRNAs (miRNAs) are emerging as key post-transcriptional regulators of a suite of signaling pathways and pathophysiological effects. Abnormalities in high number of miRNA and their associated functions have been described in several SADs, suggesting their involvement in the development of atherosclerosis and thrombosis in the setting of RA, SLE and APS. This review focusses on recent insights into the potential role of miRNAs both, as clinical biomarkers of atherosclerosis and thrombosis in SADs, and as therapeutic targets in the regulation of the most influential processes that govern those disorders, highlighting the potential diagnostic and therapeutic properties of miRNAs in the management of CVD.

Increased antibody levels to stage-specific Epstein-Barr virus antigens in systemic autoimmune diseases reveal a common pathology.

The immune responses to antigens from different stages of the Epstein-Barr virus (EBV) life cycle were investigated in systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), Sjögren's syndrome (SS), and systemic sclerosis (SSc) to gain knowledge of EBV's involvement in the etiology of systemic autoimmune diseases (SADs) and for an overview of the humoral immune responses against EBV. Investigations were performed by the use of ELISA. IgM, IgA, and IgG antibody binding to 11 EBV antigens: EBNA1, EBNA2, BALF5, EAD, BALF2, EA/R, VCA p18, VCA p23, gB, gp350, and gp42 were examined in serum pools from SAD patients and healthy controls (HCs). Increased antibody levels against the 11 EBV antigens in the SAD pools were seen compared to the HC pool. Specifically, SLE was characterized by strongly increased IgA to EAD both compared to HCs and other SADs, and RA was characterized by increased IgM levels to several EBV antigens. The SADs may be partly distinguished by their differential immune responses to various antigens in the EBV life cycle. All together, these findings support an association between EBV infection and SADs.

Systemic autoimmune diseases are associated with an increased risk of obsessive-compulsive disorder: a nationwide population-based cohort study.

PURPOSE: Studies suggested autoimmunity plays a role in the etiology of obsessive-compulsive disorder (OCD). The purpose of this study was to determine if a history of systemic autoimmune diseases (SADs) is associated with an increased risk of subsequent onset of OCD. METHODS: Patients with or without SADs were identified in the Taiwan National Health Insurance Program. The SADs cohort consisted of 63,165, while the comparison cohort consisted of 315,825 patients. The incidence rates of OCD with a maximum follow-up period of 10 years between patients with and without SADs were compared using a Cox proportional hazard model to estimate the hazard ratio (HR) and 95% confidence interval (95% CI). RESULTS: The major finding was the discovery of a higher incidence of subsequent OCD among patients with SADs (HR: 1.85; 95% CI 1.41-2.43) after adjusted for other demographic characteristics. Specifically, the risk of OCD was observed to be significant increase in systemic lupus erythematosus (1.65, 1.07-2.54) dermatomyositis (3.25, 1.04-10.17), and Sjögren's syndrome (2.38, 1.53-3.72). Also, this study revealed some potential risk factors for developing OCD, including younger age (less than or equal to 50-year-old) and some comorbidities (alcohol use disorder, liver cirrhosis, and malignancies). Conversely, this study found that steroid use was a potential protective factor for the development of OCD. CONCLUSIONS: This study confirms that SADs are associated with higher incidence of OCD, suggesting that abnormal autoimmune process is associated with increased expression of psychiatric disturbances.

An Integrated Soft Computing Approach to Hughes Syndrome Risk Assessment.

The AntiPhospholipid Syndrome (APS) is an acquired autoimmune disorder induced by high levels of antiphospholipid antibodies that cause arterial and veins thrombosis, as well as pregnancy-related complications and morbidity, as clinical manifestations. This autoimmune hypercoagulable state, usually known as Hughes syndrome, has severe consequences for the patients, being one of the main causes of thrombotic disorders and death. Therefore, it is required to be preventive; being aware of how probable is to have that kind of syndrome. Despite the updated of antiphospholipid syndrome classification, the diagnosis remains difficult to establish. Additional research on clinically relevant antibodies and standardization of their quantification are required in order to improve the antiphospholipid syndrome risk assessment. Thus, this work will focus on the development of a diagnosis decision support system in terms of a formal agenda built on a Logic Programming approach to knowledge representation and reasoning, complemented with a computational framework based on Artificial Neural Networks. The proposed model allows for improving the diagnosis, classifying properly the patients that really presented this pathology (sensitivity higher than 85%), as well as classifying the absence of APS (specificity close to 95%).

Organ Damage and Quality of Life in Antiphospholipid Syndrome.

Antiphospholipid syndrome (APS) affects young patients in the most productive years of their life, and the consequences of organic or tissue damage involve a decrease in health-related quality of life (HRQoL). While acute disease manifestations of APS are well known, information on the long-term prognosis and damage in affected patients is still very limited. Systemic lupus erythematosus (SLE) patients would be expected to experience long-term complications and even die as a consequence of APS. Organ damage in APS has been evaluated using different methods and definitions, including the SLICC/ACR Damage Index (SDI), which tend to underestimate aPL-related damage. A new damage index in APS has been proposed (DIAPS), and it seems to be more accurate than SDI. Given the implications for morbidity and mortality, it is imperative to assess accurately aPL-related damage and HRQoL in patients with APS.

Increased Serum Levels of Anti-Carbamylated 78-kDa Glucose-Regulated Protein Antibody in Patients with Rheumatoid Arthritis.

The objective of this study was to investigate the presence and titer of anti-carbamylated 78-kDa glucose-regulated protein (anti-CarGRP78) antibody in serum from controls, and patients with rheumatoid arthritis (RA), systemic lupus erythematosus (SLE) and primary Sjögren syndrome (pSS). Thirty-three RA patients, 20 SLE patients, 20 pSS patients, and 20 controls were enrolled from our outpatient clinic. GRP78 was cloned and carbamylated. Serum titers of anti- cyclic citrullinated peptides (anti-CCP), anti-GRP78, and anti-CarGRP78 were measured with an enzyme-linked immunosorbent assay. No differences in serum titers of anti-GRP78 antibody in patients with RA, SLE, or pSS compared with the controls were observed. Serum levels of anti-carGRP78 antibody in patients with RA, but not SLE or pSS, were significantly higher compared with the controls (OD405 0.15 ± 0.08 versus 0.11 ± 0.03, p = 0.033). There was a positive correlation between the serum levels of anti-GRP78 antibody, but not anti-CarGRP78 antibody, with the levels of anti-CCP antibody in patients with RA. Both anti-GRP78 and anti-carGRP78 antibodies failed to correlate with C-reactive protein levels in patients with RA. In conclusion, we demonstrated the presence of anti-CarGRP78 antibody in patients with RA. In addition, the serum titer of anti-CarGRP78 antibody was significantly elevated in patients with RA compared with the controls. Anti-CarGRP78 antibody could also be detected in patients with SLE or pSS.

High risk of misclassification of acute Parvovirus B19 infection into a systemic rheumatic disease.

Objectives: Parvovirus B19 most frequently causes epidemics of erythema infectiosum in children but also affects adults often leading to rheumatologic manifestations. While the serum profile allows the diagnosis, manifestations may mimic autoimmune conditions. The aim was to evaluate the proportion of patients with acute Parvovirus B19 infection fulfilling classification criteria for rheumatic diseases (RA and SLE). Methods: We evaluated the clinical and serological features of 54 patients diagnosed with acute Parvovirus B19 infection seeking rheumatological attention between March and June 2024. Results: The majority of patients were females (78%), with a mean (s.d.) age of 45 (13) years and 54% could not recall any known exposure. Fifty-one/54 (94%) had arthralgia, 27 (50%) arthritis (oligoarthritis in 67% of them), 24 (44%) fever, 19 (35%) skin rash and 7 (13%) purpura. Symptoms resolution generally occurred within 6 weeks. Complement levels were low in 14/33 (42%) tested patients, while the presence of serum ANA, anti-dsDNA, anti-phospholipids and rheumatoid factor was detected in 21/38 (55%), 10/26 (38%), 6/12 (50%) and 5/37 (13%) patients, respectively. Classification criteria for SLE were fulfilled in 93% of ANA-positive patients and RA criteria in 38% of patients with arthritis. Conclusions: Parvovirus B19 infection manifestations may vary and nearly all patients with positive serum ANA fulfil the classification criteria for SLE. The risk of misclassification in patients with viral infection should not be overlooked.

CD19 Chimeric Antigen Receptor (CAR) T-Cell Therapy for Systemic Autoimmune Diseases.

A small number of drugs have been the sole stay of conventional treatment for autoimmune illnesses for the past 10 years. These medications have a number of side effects that restrict their usage and necessitate continuous administration to keep a patient in a state of remission. While many new treatments are being researched to address this problem, chimeric antigen receptor (CAR) T-cell therapy currently shows the greatest potential. Current medical guidelines do not currently advocate the use of this medicine because it is still in its early stages of development due to continuing clinical research. Therefore, the aim of this systematic review was to determine what new findings have been reported in recent studies about the safety and efficacy of CAR T-cells. From the nine studies collected in total, it was found that systemic lupus erythematosus (SLE) was the most often researched autoimmune disease. The CAR T-cell therapy had noticeable results after one to two months on average. The most frequent adverse effect was cytokine release syndrome (CRS), which was treated cautiously and infrequently necessitated extensive intervention. All serological tests showed improvement, and clinical remission was always achieved. This review concludes that, due to the one-time infusion and low adverse reaction rate, the therapy not only outperforms conventional drugs but is also more practical. There is even more cause to look forward to the full deployment of this innovative therapeutic alternative, as variations of the therapy are currently being explored.

Reflecting on a decade of the international consensus on ANA patterns (ICAP): Accomplishments and challenges from the perspective of the 7th ICAP workshop.

The International Consensus on ANA Patterns (ICAP) is an ongoing international initiative dedicated to harmonizing technical and interpretation aspects of the HEp-2 IFA test. Comprised of internationally recognized experts in autoimmunity and HEp-2 IFA testing, ICAP has operated for the last 10 years by promoting accurate reading, interpretation, and reporting of HEp-2 IFA images by professionals involved in various areas related to autoimmune diseases, such as clinical diagnostic laboratories, academic research, IVD industry, and patient care. ICAP operates through continuous information exchange with the international community and encourages the participation of younger experts from all over the world. The 7th ICAP workshop has addressed several aspects that originated from this interaction with the international community and has effectively established objective goals and tasks to be delivered over the next two years. Some of these are outlined in this article, including the planning of three audio-visual educational modules to be posted at the www.anapattern.org website, the classification of two novel HEp-2 IFA patterns, the implementation of a project dedicated to continuously updating the information on the clinical and immunologic relevance of the HEp-2 IFA patterns, and the launch of two additional branches of the HEp-2 Clinical and Immunological (HEp-2 CIC) project.