Autoimmunity最新文献

{"title":"SARS-CoV-2 spike-specific regulatory T cells (Treg) expand and develop memory in vaccine recipients suggesting a role for immune regulation in preventing severe symptoms in COVID-19.","authors":"Alessandra Franco, Jaeyoon Song, Christina Chambers, Alessandro Sette, Alba Grifoni","doi":"10.1080/08916934.2023.2259133","DOIUrl":"10.1080/08916934.2023.2259133","url":null,"abstract":"<p><p>We enrolled healthy subjects that received 2 to 4 injections of mRNA-based vaccination to prevent COVID-19 months to a year from the last vaccine boost, and we found numerous SARS-CoV-2 spike-specific regulatory T cell (Treg) that developed T cell memory as effector memory T cells (T_EM) and central memory T cells (T_CM). CD4+ CD25^high Treg expressed the chemokine receptor CCR6 in a considerable percentage, suggesting T cell homing to the vascular endothelium, lung and gut epithelial cells and brain. Treg phenotype was different than peripherally-induced Treg (pTreg) that revert from pro-inflammatory T cells under repeated stimulatory conditions, suggesting that SARS-CoV-2 spike-specific Treg differentiated from naïve T cells in tissues where the SARS-CoV-2 spike proteins were synthetized. Twenty two of 22 subjects studied responded to vaccination developing a spike-specific CD4+ T helper (Th)1 response, and 20 of 22 developing a spike-specific CD8+ cytotoxic T cells (CTL) response. However, in vaccine recipients the expansion of spike-specific pro-inflammatory T cells was less significant than the expansion of spike-specific Treg. Effector (T_EM) and central memory (T_CM) Treg were numerous as early as after two vaccine doses, with no significant differences following additional vaccine boosts. In co-culture experiments under stimulatory conditions, Treg regulated naïve T cell differentiation toward a pro-inflammatory phenotype and suppressed interferon (IFN)γ production by SARS-CoV-2-specific CD4 + Th1 cells.</p>","PeriodicalId":8688,"journal":{"name":"Autoimmunity","volume":"56 1","pages":"2259133"},"PeriodicalIF":3.5,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41103180","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mesenchymal stem cells-derived exosomes ameliorate high glucose and lipopolysaccharide-induced HPMECs injury through the Nrf2/HO-1 pathway","authors":"Hongyan Sun, Shitao Lu, Gaowei Qu, Junli Li, Bo Song","doi":"10.1080/08916934.2023.2290357","DOIUrl":"https://doi.org/10.1080/08916934.2023.2290357","url":null,"abstract":"Abstract Mesenchymal stem cells-derived exosomes (MSC-Exo) are considered to have great potential in the treatment of human diseases. However, the role of MSC-Exo in the process of diabetes with sepsis and the underlying molecular mechanism remain unclear. Human pulmonary microvascular endothelial cells (HPMECs) were treated with high glucose (HG) and lipopolysaccharide (LPS). Cell viability, migration, angiogenesis were analyzed by cell counting kit 8 assay, transwell assay and tube formation assay. Transmembrane electrical resistance (TER) detection and FITC-dextran assay were performed to evaluate cell barrier function. The protein levels of cell permeability-related markers, ferroptosis-related markers, exosomes-related markers, Nrf2 and HO-1 were examined using western bolt (WB) analysis. Besides, the levels of inflammation factors were tested by ELISA, and the levels of ferroptosis-related indicators were examined using corresponding assay kits. Flow cytometry was employed to analyze stem cell markers. The identification of MSC-Exo was performed using transmission electron microscopy, nanoparticle tracking analysis and WB analysis. DIO staining was used to examine the uptake of MSC-Exo by HPMECs. HG treatment suppressed HPMECs viability, migration, angiogenesis and TER, while promoted permeability, inflammation and ferroptosis. LPS treatment aggravated HG-induced HPMECs dysfunction, inflammation and ferroptosis. After HPMECs were co-cultured with MSC-Exo, cell injury induced by HG + LPS could be relieved. Moreover, MSC-Exo treatment enhanced the activity of Nrf2/HO-1 pathway in HG + LPS-induced HPMECs, and Nrf2-silenced MSC-Exo could promote HG + LPS-induced HPMECs injury. MSC-Exo alleviated HG + LPS-induced HPMECs injury via activating Nrf2/HO-1 pathway, confirming that it might be used for the treatment of diabetes with sepsis.","PeriodicalId":8688,"journal":{"name":"Autoimmunity","volume":"53 s42","pages":""},"PeriodicalIF":3.5,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138627691","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circ_0035796 depletion inhibits transforming growth factor-β1-induced pulmonary fibrosis in a miR-150-5p/L1CAM-dependent manner.","authors":"Juan Li, Xiaohong Chen, Baohong Zhang, Chenlu Wang","doi":"10.1080/08916934.2023.2250099","DOIUrl":"10.1080/08916934.2023.2250099","url":null,"abstract":"<p><strong>Background: </strong>The pathogenesis of pulmonary fibrosis is not fully understood. Previous work has demonstrated the important role of circular RNA (circRNA) in pulmonary fibrosis development. This study aims to analyse the role of circ_0035796 in pulmonary fibrosis and the underlying mechanism.</p><p><strong>Methods: </strong>Human foetal lung fibroblast 1 (HFL1) cells were treated with transforming growth factor-β1 (TGF-β1) to mimic a pulmonary fibrosis cell model. The expression of circ_0035796, microRNA-150-5p (miR-150-5p) and L1 cell adhesion molecule (L1CAM) was determined by quantitative real-time polymerase chain reaction (qRT-PCR). The protein expression of L1CAM, collagen I and fibronectin was detected by Western blot. Cell viability was analysed by CCK-8 assay. Cell proliferation, invasion and migration were investigated by 5-Ethynyl-2'-deoxyuridine (EdU) assay, transwell invasion assay and wound-healing assay, respectively. The secretion of interleukin-6 (IL-6) and tumour necrosis factor-α (TNF-α) was analysed by Enzyme-linked immunosorbent assay (ELISA). Oxidative stress was assessed by detecting Superoxide Dismutase (SOD) activity and Malondialdehyde (MDA) level using commercial kits. The association of miR-150-5p with circ_0035796 and L1CAM was identified by dual-luciferase reporter assay, RNA pull-down assay and RNA immunoprecipitation (RIP) assay.</p><p><strong>Results: </strong>Circ_0035796 and L1CAM expression were dramatically upregulated, while miR-150-5p expression was downregulated in TGF-β1-treated HFL1 cells. TGF-β1 treatment induced cell proliferation, migration, invasion, IL-6 and TNF-α secretion, and oxidative stress, whereas circ_0035796 depletion relieved these effects. In addition, circ_0035796 acted as a sponge of miR-150-5p and miR-150-5p combined with L1CAM. Moreover, miR-150-5p depletion attenuated circ_0035796 knockdown-mediated effects in TGF-β1-exposed HFL1 cells. The regulation of miR-150-5p on TGF-β1-induced fibroblast activation involved the downregulation of L1CAM. Further, circ_0035796 modulated L1CAM expression by interacting with miR-150-5p in TGF-β1-exposed HFL1 cells.</p><p><strong>Conclusion: </strong>Circ_0035796 knockdown ameliorates TGF-β1-induced pulmonary fibrosis through the miR-150-5p/L1CAM axis <i>in vitro</i>.</p>","PeriodicalId":8688,"journal":{"name":"Autoimmunity","volume":"56 1","pages":"2250099"},"PeriodicalIF":3.5,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41189667","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Regulatory role of ceRNA network in B lymphocytes of patients with immune thrombocytopenia.","authors":"Xin He, Nianbin Li, Donglan Liu, Mengtong Zang, Manjun Zhao, Ningyuan Ran, Chunyan Liu, Limin Xing, Huaquan Wang, Ting Wang, Zonghong Shao","doi":"10.1080/08916934.2023.2281225","DOIUrl":"10.1080/08916934.2023.2281225","url":null,"abstract":"<p><strong>Objective: </strong>High-throughput sequencing was used to screen expressing differences of miRNA, lncRNA, and mRNA in CD19+ B peripheral blood samples of newly diagnosed immune thrombocytopenia (ITP) patients and healthy controls. The study aimed to explore the regulatory role of ceRNA network in the pathogenesis of dysfunctional CD19 + B lymphocytes of ITP patients.</p><p><strong>Methods: </strong>CD19+ B lymphocytes were isolated from peripheral blood samples of ITP patients and their healthy counterparts. High-throughput sequencing was used to screen for the expression of miRNA, lncRNA, and mRNA of ITP patients and healthy controls, which were analysed by the ceRNA network. Moreover, qPCR was used to verify the differential expression of miRNA, lncRNA, and mRNA in ITP patients and healthy controls. The correlation between differentially expressed miRNA, lncRNA, mRNA, and B lymphocyte subsets was also analysed.</p><p><strong>Results: </strong>The CD19+ B lymphocytes of 4 newly diagnosed ITP patients and 4 healthy controls were sequenced and analysed. There were 65 differentially expressed lncRNA and 149 mRNA forming a ceRNA network showed that 12 lncRNA and 136 differentially expressed mRNA were closely associated. Similarly, miR-144-3p, miR-374c-3p, and miR-451a were highly expressed in ITP patients, as confirmed by qPCR, which was consistent with the high-throughput sequence results. LOC102724852 and CCL20 were highly expressed in ITP patients, while LOC105378901, LOC112268311, ALAS2, and TBC1D3F were not as compared to healthy controls, which was consistent with the high-throughput sequence results. In addition, the expression of miR-374c-3p, LOC112268311, LOC105378901, and CXCL3 were correlated with the percentage of B lymphocyte subsets.</p><p><strong>Conclusions: </strong>The ceRNA network of miRNA, lncRNA, and mRNA in peripheral CD19 + B lymphocytes plays an essential role in the pathogenesis of ITP.</p>","PeriodicalId":8688,"journal":{"name":"Autoimmunity","volume":"56 1","pages":"2281225"},"PeriodicalIF":3.5,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138486565","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hypoxic tumour-derived exosomal miR-1225-5p regulates M2 macrophage polarisation via toll-like receptor 2 to promote ovarian cancer progress.","authors":"Shu Tan, Hao Yu, Zhaocong Zhang, Yiming Liu, Ge Lou","doi":"10.1080/08916934.2023.2281226","DOIUrl":"10.1080/08916934.2023.2281226","url":null,"abstract":"<p><p>Tumor-secreted exosomes are critical for the functional regulation of tumor-associated macrophages (TAMs). This study aimed to explore how exosomes secreted by ovarian carcinoma cells regulate the phenotype and function of macrophages. Hypoxic treatment of A2780 cells was postulated to mimic the tumor microenvironment, and exosomes were co-cultured with TAMs. miR-1225-5p was enriched in hypoxic exosomes and contributed to M2 macrophage polarizationby modulating Toll-like receptor 2 expression (TLR2). Furthermore, hypoxia-treated macrophages promote ovarian cancer cell viability, migration, and invasion via the wnt/β-catenin pathway. This study clarified that exosomal miR-1225-5p promotes macrophage M2-like polarization by targeting TLR2 to promote ovarian cancer, which may via the wnt/β-catenin pathway.</p>","PeriodicalId":8688,"journal":{"name":"Autoimmunity","volume":"56 1","pages":"2281226"},"PeriodicalIF":3.5,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138443619","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of Agmatine on a mouse model of allergic airway inflammation: A comparative study.","authors":"Mohammed K Еlmahdy,&nbsp;Rania R Abdelaziz,&nbsp;Hoda S Elmahdi,&nbsp;Ghada M Suddеk","doi":"10.1080/08916934.2022.2093864","DOIUrl":"https://doi.org/10.1080/08916934.2022.2093864","url":null,"abstract":"<p><strong>Introduction: </strong>Asthma is a chronic lung disease that injures and constricts the airways. This study evaluates the effects of agmatine on ovalbumin (OVA)-induced allergic inflammation of the airways.</p><p><strong>Methods: </strong>OVA sensitization by intraperitoneal injection was used to induce airway inflammation in mice on days 0 and 7; then the mice were challenged using beclomethasone (150 µg/kg, inhalation), a standard anti-asthmatic drug, from day 14 to day 16. Furthermore, agmatine (200 mg/kg) was intraperitoneally injected on day 0 and then daily for 16 days, followed by OVA challenge. The lung weight ratio, total and differential cell counts, TNF-α, interleukin-5 (IL-5) and IL-13 in bronchoalveolar lavage fluid (BALF), lung nitrite/nitrate (NO), and oxidative parameters were determined. Moreover, histopathological and immunohistochemical staining was employed.</p><p><strong>Results: </strong>Injection of agmatine (200 mg/kg) for 16 days significantly attenuated inflammation of the airways. The levels of BALF inflammatory cells, TNF-α, IL-5, IL-13, lung NO, and malondialdehyde (MDA), significantly decreased with concomitant elevation of superoxide dismutase (SOD) levels. Histological and immunohistochemical analyses of mast cells paralleled to biochemical improvements.</p><p><strong>Conclusion: </strong>Finally, this study illustrated that agmatine attenuates the allergic inflammation of airways caused by OVA by mitigating cytokines release, NO expression, and oxidative stress.</p>","PeriodicalId":8688,"journal":{"name":"Autoimmunity","volume":"55 8","pages":"608-619"},"PeriodicalIF":3.5,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9517835","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Functional significance of the rare rs35667974 <i>IFIH1</i> gene polymorphism, associated with multiple autoimmune diseases, using a structural biological approach.","authors":"Maria I Zervou,&nbsp;Athena C Andreou,&nbsp;Elias E Eliopoulos,&nbsp;George N Goulielmos","doi":"10.1080/08916934.2022.2103799","DOIUrl":"https://doi.org/10.1080/08916934.2022.2103799","url":null,"abstract":"<p><p>Autoimmune diseases, which affect approximately 5% of human population, are a range of diseases in which the immune response to self-antigens results in damage or dysfunction of tissues. Recent genome wide association studies (GWAS) have successfully identified novel autoimmune disease-associated loci, with many of them shared by multiple disease-associated pathways but much of the genetics and pathophysiological mechanisms remain still obscure. Considering that most of the potential causal variants are still unknown, many studies showed that the missense variant rs35667974 at interferon-induced with helicase C domain 1 (<i>IFIH1</i>) gene is protective for type 1 diabetes (T1D), psoriasis (PS) and psoriatic arthritis (PsA). Recently, this variant was found to be also associated with ankylosing spondylitis (AS), Crohn's disease (CD) and ulcerative colitis (UC). The <i>IFIH1</i> gene encodes a cytoplasmic RNA helicase otherwise known as melanoma differentiation-associated 5 (MDA5) that recognizes viral RNA and is involved in innate immunity through recognition of viral RNA. In the present study we sought to investigate the association of the rare rs35667974 variant of <i>IFIH1</i> gene, which resides in exon 14 and changes a conserved isoleucine at position #923 to valine, in the development of various autoimmune diseases and give a reason for the selectivity affecting different autoimmune diseases. Evolutionary studies and three-dimensional (3 D) homology modelling were employed on the MDA5 protein product, through its association with dsRNA, recognition factor controlling cytokine and chemokine signalling, to investigate the protective role of the MDA5 variant for certain autoimmune diseases.</p>","PeriodicalId":8688,"journal":{"name":"Autoimmunity","volume":"55 7","pages":"455-461"},"PeriodicalIF":3.5,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40664705","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circ_0114428 promotes proliferation, fibrosis and EMT process of high glucose-induced glomerular mesangial cells through regulating the miR-185-5p/SMAD3 axis.","authors":"Bo Li,&nbsp;Guijiang Sun,&nbsp;Haibo Yu,&nbsp;Jia Meng,&nbsp;Fang Wei","doi":"10.1080/08916934.2022.2103797","DOIUrl":"https://doi.org/10.1080/08916934.2022.2103797","url":null,"abstract":"<p><p>Circular RNA (circRNA) has been confirmed to be the key regulators of diabetic nephropathy (DN) progression. However, the role of circ_0114428 in the DN progression remains unclear. Glomerular mesangial cells (GMCs) were treated with high glucose (HG) to mimic DN cell models <i>in vitro</i>. The expression levels of circ_0114428, microRNA (miR)-185-5p, and SMAD3 mRNA were examined by quantitative real-time PCR. Cell proliferation ability was detected by MTT assay, EdU staining and flow cytometry. The protein levels of proliferation marker, fibrosis markers, epithelial-mesenchymal transition (EMT) markers and SMAD3 were measured by western blot assay. The interaction between miR-185-5p and circ_0114428 or SMAD3 was confirmed <i>via</i> dual-luciferase reporter assay, RIP assay and RNA pull-down assay. Our data showed that circ_0114428 was upregulated in HG-induced GMCs. Circ_0114428 overexpression could aggravate the promotion effect of HG on the proliferation, fibrosis and EMT process of GMCs, while its knockdown had an opposite effect. In the terms of mechanisms, circ_0114428 could sponge miR-185-5p to regulate SMAD3. MiR-185-5p inhibitor could reverse the suppressive effect of circ_0114428 knockdown on the proliferation, fibrosis and EMT process in HG-induced GMCs. Also, SMAD3 overexpression abolished the inhibition of miR-185-5p on the proliferation, fibrosis and EMT process in HG-induced GMCs. Taken together, our data suggested that circ_0114428 might promote DN progression by regulating the miR-185-5p/SMAD3 axis.</p>","PeriodicalId":8688,"journal":{"name":"Autoimmunity","volume":"55 7","pages":"462-472"},"PeriodicalIF":3.5,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40540190","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction.","authors":"","doi":"10.1080/08916934.2022.2103273","DOIUrl":"https://doi.org/10.1080/08916934.2022.2103273","url":null,"abstract":"","PeriodicalId":8688,"journal":{"name":"Autoimmunity","volume":"55 7","pages":"I"},"PeriodicalIF":3.5,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40521464","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Abnormal lower expression of GPR183 in peripheral blood T and B cell subsets of systemic lupus erythematosus patients.","authors":"Mingming Zhao,&nbsp;Yang Mei,&nbsp;Zhidan Zhao,&nbsp;Pengpeng Cao,&nbsp;Yue Xin,&nbsp;Yunkai Guo,&nbsp;Ming Yang,&nbsp;Haijing Wu","doi":"10.1080/08916934.2022.2103119","DOIUrl":"https://doi.org/10.1080/08916934.2022.2103119","url":null,"abstract":"<p><p>G protein-coupled receptor 183 (GPR183) has been indicated to mediate the migration and localisation of immune cells in T cell-dependent antibody responses. Systemic lupus erythematosus (SLE) is a canonical autoimmune disease involving B cell-mediated tolerance destruction and excessive pathogenic autoantibody production, in which multiple GPCRs play a role. To date, there has been no systematic study regarding the expression of GPR183 in lymphocyte subsets of SLE patients. In this research, firstly, we observed the expression trends of GRP183 in various T and B cell subsets in human tonsil tissues. These lymphocyte subsets include CD4⁺, CD8⁺, naïve T, effector T, Tfh, activated Tfh, Th1, Th2, Th17, Treg, CD19⁺CD27^-, CD19⁺CD27⁺, naïve B, germinal centre B, memory B, and plasma cells. Further, compared with healthy controls (HCs), GPR183 expression levels in above peripheral blood lymphocyte subsets of patients with SLE were reduced overall. The differential expression of GPR183 expression between inactive and active SLE patients indicates that GPR183 expression may be concerned with the disease activity of SLE. This was further confirmed through the strong negative correlation with SLEDAI score and positive correlation with serum complement protein C3, C4 and C1q levels. Further receiver operating characteristic (ROC) curve analysis revealed that GPR183 expression in circulating CD27^-IgD⁺ B cells may be beneficial in distinguishing between inactive and active SLE patients. In addition, type I interferon stimulation could down-regulate the expression of GPR183 in peripheral blood T and B cell subsets. Aberrant expression of GPR183 may provide some novel insights into disease activity prediction and underlying pathogenesis of SLE.</p>","PeriodicalId":8688,"journal":{"name":"Autoimmunity","volume":"55 7","pages":"429-442"},"PeriodicalIF":3.5,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40537098","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}