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The article focuses on a study which compares antisynthetase syndrome (ASS) cases with hyperferritinaemia to those without hyperferritinaemia to reveal their characteristics. Topics discussed include the presence anti-aminoacyl-tRNA synthetase (ARS) antibodies in some patients with inflammatory myopathy or myositis, the definition of hyperferritinaemia, and the association of hyperferritinaemia in ASS with evident myositis, systemic inflammation, anti-EJ antiboides, and malignancy.

Discovered in China in December 2019, coronavirus disease-19 (COVID-19) has confronted the world with an unprecedented crisis. Healthcare workers, the first line of defense against this pandemic, have been severely affected. Clinical trial results of the emergency vaccines showed that they all produced IgG antibodies against severe acute respiratory syndrome corona virus-2 (SARS-CoV-2) with high rates of seroconversion. While immunization against natural challenge (COVID-19 infection) and artificial challenge (vaccination) in health care workers is relatively well described in the West, the issue is not well understood in Sub-Saharan Africa, particularly in Côte d'Ivoire, where populations are genetically distinct from Caucasians. Our aim was to investigate the magnitude of post-vaccination IgG responses to SARS-CoV-2 in healthcare workers in our African epigenetic context. A cross-sectional, multicenter, analytical study was conducted from March to May 2022 among health workers employed at the University Hospital of Abidjan and vaccinated against COVID-19. The study included 77 health workers. IgG immunoassays were performed with an enzyme-linked fluorescent assays. Data were analyzed using SPSS version 22.0 software, with a p-value ˂ 0.05 considered as a significant difference. All enrolled subjects developed anti-SRAS-Cov-2 IgG, of which 88.3% had a strong response (titer ≥ 250 Binding Antibody Units/ml). IgG titers varied significantly by gender (p=0.04). Vaccine type and number of doses did not affect IgG titers. However, a history of COVID-19 infection was associated with a 5-fold greater likelihood of developing a strong IgG response after vaccination. In conclusion, humoral IgG responses developed after vaccination against SARS-CoV-2 were robust and would be influenced by a variety of factors.., (Copyright© by the Egyptian Association of Immunologists.)

Respiratory manifestations related to the intake of non-steroidal anti-inflammatory drugs (NSAIDs) during the treatment of the painful vaso-occlusive crisis of sickle cell disease are either a type I hypersensitivity mechanism of the Gell and Coombs classification, or a pharmacological mechanism of NSAIDs. The use of NSAIDs is essential in the Abidjan school because of the absence of therapeutic alternatives in the management of the inflammatory crisis of this disease. The induction of tolerance to NSAIDs initiated by the authors has had clear clinical success. The basic biological reasons for this tolerance were evaluated in this study. A group of 11 sickle cell patients aged 12 to 39 years in whom post-NSAID respiratory manifestations disappeared for at least 6 months following a short tolerance induction protocol with ibuprofen, was assayed by ELISA for TNFα, INF (Th1 cytokines), IL-4 (Th2 cytokine), IL-10, TGF-β (immunosuppressive cytokines) and total IgE, before induction or pre-induction (D-1) and at day one (D1), D2- 3, one month (M1), and M6 after induction. A repolarization of the Th1/Th2 balance was noted during the post induction period. The high concentration of IL-4 observed at D-1 gradually decreased in favor of the cytokines TNFα, INF. The decrease in cytokine IL-4 with the level of total IgE was accompanied by the increase of IL-10 and TGF-β demonstrating the regulatory role of these cytokines in the control of allergic diseases. In conclusion, the induction of immuno-tolerance to NSAIDs through a short protocol is well supported by immune regulation. The medium-term effects are real, unlike the results of allergen desensitization or specific immunotherapy. However, this protocol could be used in certain circumstances such as in the case of intolerance to trimethoprim-sulfamethoxazole, used as the treatment of choice for the prevention of opportunistic diseases in people living with human immunodeficiency virus., (Copyright© by the Egyptian Association of Immunologists.)

Recently, a certain volume of biopsy specimens has been required for genetic testing of tumors using endobronchial ultrasound-guided transbronchial needle aspiration (EBUS-TBNA). This study aimed to verify the superiority of our newly devised EBUS-TBNA biopsy technique, the "cross-fanning technique," which combines rotation and up-down maneuvers, by comparing its harvest volume with that of other maneuvers. Using a bronchoscope simulator, ultrasonic bronchoscope, and 21-gauge puncture needle, we compared the weight of silicone biopsy specimens obtained by the following 4 procedures: Conventional maneuver; Up-down maneuver; Rotation maneuver, and; Cross-fanning technique. Each procedure was repeated 24 times in total, rotating the sequences of the maneuvers, and the operator/assistant pair to align the conditions. The means ± standard deviations of the sample volumes for each puncture technique were as follows: 2.8 ± 1.2 mg; 3.1 ± 1.6 mg; 3.7 ± 1.2 mg, and; 3.9 ± 1.2 mg. There was a significant difference between the 4 groups (P = .024). The post hoc test showed a statistically significant difference between techniques A and D (P = .019). This study showed that the cross-fanning technique might contribute to the increased volume of tissue samples obtained by EBUS-TBNA biopsy., Competing Interests: The authors have no funding and conflicts of interest to disclose., (Copyright © 2023 the Author(s). Published by Wolters Kluwer Health, Inc.)

The consecutive reports and stored images of ultrasound examinations for 100 symptomatic ankles of 74 patients with rheumatoid arthritis (RA) were reviewed for the presence or absence of retrocalcaneal bursitis (RCB) and Achilles tendon enthesitis (ATE). The ankles were classified into 4 categories based on the presence or absence of RCB or ATE. The number of RCB(-)/ATE(-), RCB(+)/ATE(-), RCB(+)/ATE(+), and RCB(-)/ATE(+) ankles was 62, 16, 12, and 10, respectively. When classifying patients into early RA and established RA, the percentage of RCB(-)/ATE(+) ankles with early RA was significantly lower than that with established RA ( P  = .00595). The disease duration was significantly longer in the RCB(-)/ATE(+) ankles than in the RCB(+)/ATE(-) ankles (median [interquartile range]: 15.29 [8.69] months vs 3.6 [3.06] months, P  = .0247). It was speculated that RCB precedes or accompanies ATE in the early phase of RA, which suggests that entheseal inflammation in RA arises from synovial tissues., Competing Interests: Declaration of conflicting interests:The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Semiquantitative scoring for subacromial bursa (SAB), subdeltoid bursa (SDB), and subcoracoid bursa by both gray-scale (GS) and power Doppler (PD) ultrasonography was performed in 15 patients with polymyalgia rheumatica (PMR) (72.6 ± 7.7 years old) and 15 patients with elderly onset rheumatoid arthritis with PMR-like onset (pm-EORA) (70.7 ± 7.0 years old) before starting treatment. The GS grades of SAB were significantly higher in the shoulders with pm-EORA than in the shoulders with PMR. The GS and PD scores of SAB and the PD scores of SDB were significantly higher in pm-EORA than in PMR cases. The sums of GS and/or PD scores for the three bursae were significantly higher in pm-EORA than in patients with PMR. The sums of GS and PD scores for SAB were significantly higher in pm-EORA than in PMR cases. Moderate to severe proliferative synovitis of the shoulder bursae, especially in SAB, is a key feature for discriminating pm-EORA from PMR., Competing Interests: Declaration of conflicting interests:The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

A 59-year-old man who presented with continuous fever, livedo reticularis, and left leg ischemia with multiple tibial artery stenosis and renal artery aneurysm, as demonstrated by arteriography, was diagnosed with polyarteritis nodosa (PAN) 6 years ago. Although he frequently relapsed in spite of intensive immunosuppressive therapies, the disease activity of PAN was controlled with repeated rituximab (RTX) therapies and steroid doses were tapered safely. Peripheral CD19 + B-cells disappeared soon after the 1st administration of RTX. Although CD19 + B-cells remained absent, 3.1% of CD3 + CD20 + T-cells were observed in the peripheral blood prior to the 2nd administration of RTX. Recent studies have suggested the pathogenic role of CD3 + CD20 + T-cells in autoimmune diseases in the context of RTX therapy; therefore, their roles in the pathogenesis of PAN also need to be considered.

Objectives . To develop a scoring system for evaluating the extrasynovial soft tissue inflammation of the shoulders in patients with polymyalgia rheumatica (PMR) and elderly-onset rheumatoid arthritis with PMR-like onset (pm-EORA) using ultrasound. Methods . We analyzed stored power Doppler (PD) images obtained by the pretreatment examination of 15 PMR patients and 15 pm-EORA patients. A semiquantitative scoring system for evaluating the severity of PD signals adjacent to the anterior aspect of the subscapularis tendon was designed. Results . A four-point scale scoring for the hyperemia on the subscapularis tendon was proposed as follows in brief: 0 = absent or minimal flow, 1 = single vessel dots or short linear-shape signals, 2 = long linear-shape signals or short zone-shape signals, or 3 = long zone-shape signals. This scoring system showed good intra- and interobserver reliability and good correlation to quantitative pixel-counting evaluation. By using it, we demonstrated that inflammation in PMR is dominantly localized in extrasynovial soft tissue as compared with pm-EORA. Conclusions . We proposed a reliable semiquantitative scoring system using ultrasound for the evaluation of extrasynovial soft tissue inflammation of the shoulders in patients with both PMR and pm-EORA. This system is simple to use and can be utilized in future investigations., Competing Interests: The authors declare that they have no competing interests.

Background: Peptidylarginine deiminase type 4 (PADI4) has been identified as a susceptibility gene for rheumatoid arthritis (RA) by genome-wide association studies. PADI4 is highly expressed in the bone marrow, macrophages, neutrophils, and monocytes. Peptidyl citrulline is an interesting molecule in RA because it is a target antigen for anti-citrullinated peptide antibodies, and only PADs (translated proteins from PADI genes) can provide peptidyl citrulline via the modification of protein substrates. The aim of this study was to evaluate the importance of the PADI4 gene in the progression of RA., Methods: We generated Padi4 knockout (Padi4(-/-)) DBA1J mice. The Padi4(-/-) DBA1J and wild-type mice were immunized with bovine type II collagen (CII) to develop collagen-induced arthritis (CIA). The expression of various inflammatory cytokines and Padi genes in immune cells was detected by the real-time TaqMan assay. Cytokine concentrations in sera were measured by enzyme-linked immunosorbent assays. Localization of the PAD4 and PAD2 proteins was indicated by immunohistochemistry., Results: We demonstrated that the clinical disease score was significantly decreased in the Padi4(-/-) mice and Padi4 expression was induced by CII immunization. In the Padi4(-/-) mice, serum anti-type II collagen (CII) immunoglobulin M (IgM), IgG, and inflammatory cytokine levels were significantly decreased compared with those in the wild-type mice. Padi2 expression was induced in the immune cells of the Padi4(-/-) mice as a compensation for the defect in Padi4., Conclusions: Padi4 affected disease severity in the CIA mice and was involved in the enhancement of the collagen-initiated inflammatory responses.

Peptidyl arginine deiminase 4 (PAD4) is an enzyme that is involved in protein citrullination, and is a target for anti-citrullinated peptide antibodies (ACPAs) in rheumatoid arthritis (RA). Genetic polymorphisms in the PADI4 gene encoding PAD4 are associated with RA susceptibility. We herein analyzed the roles of PADI4 in inflammatory arthritis using a glucose-6-phosphate isomerase (GPI)-induced arthritis (GIA) model in Padi4 knockout (KO) mice. Arthritis severity, serum anti-GPI antibody titers, and IL-6 concentrations were significantly reduced in Padi4 KO mice. The frequency of Th17 cells was decreased in GPI-immunized Padi4 KO mice, whereas WT and Padi4-deficient naïve CD4(+) T cells displayed the same efficiencies for Th17 cell differentiation in vitro. In addition, the numbers of myeloid lineage cells were reduced with the increased expression of pro-apoptotic genes in GPI-immunized Padi4 KO mice. Furthermore, the survival of Padi4-deficient neutrophils was impaired in vitro. Our results suggest that PADI4 exacerbates arthritis with diverse immunological modifications.

Rheumatoid arthritis (RA) is one of the representative auto-immune diseases, characterized by systemic inflammatory synovitis. Various genetic and environmental factors which contribute to RA pathogenesis, has been suggested, however, detailed mechanism remained unknown. While around 100 genetic risk factors for RA have been reported, Peptidylarginine deiminase type4 (PADI4) was firstly identified as a non-MHC RA genetic risk factor. Furthermore, PADI4 risk allele possessed the association with bone damage regardless of anti citrullinated peptide antibody (ACPA) positivity in Asian RA patients. PADI4 gene codes PAD4 protein which has post-translational modification activity (citrullination). Padi4 is mainly expressed in myeloid cells and granulocytes. PADI4 RA risk haplotype showed an increase of mRNA stability, which resulted in excess translation into PAD4 protein. According to ACPA specificity for RA, increasing PADI4 mRNA stability suggested a hypothesis that excess expression of PAD4 induces a large amount of citrullinated protein, which causes the induction of ACPA. On the other hand, PADI4 has nuclear trans-locational signals and is associated with regulation of various gene expression and formation of neutrophil extracellular traps. These information provide the possibility that PADI4 contributes to not only excess citrullinated protein production, but also various roles in the immune system. We summarize PADI4 function in the immune system and discuss PADI4 roles in RA.

The ability to judge the passage of time is critical to behavioral regulation and planning and can be impaired among individuals with attention deficit. Time estimation was tested in young adults screened for attention deficit, based on scores of a self-report questionnaire for attention problems (CAARS), using a prospective reproduction paradigm. Four time intervals (3, 6, 12, and 24 s) were tested in two conditions: (1) reproduction of the duration of a visual stimulus and (2) reproduction of an empty time interval. A significant interaction between gender and group was found suggesting that males, but not females, with attention deficits made larger errors than controls. Males with attention deficits and both groups of females made larger underestimations of time judgement than control males.