Autoimmunity最新文献

{"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}

{"title":"AIM2-inflammasome role in systemic lupus erythematous and rheumatoid arthritis.","authors":"E E Uresti-Rivera,&nbsp;M H García-Hernández","doi":"10.1080/08916934.2022.2103802","DOIUrl":"https://doi.org/10.1080/08916934.2022.2103802","url":null,"abstract":"<p><p>The inflammasome AIM2 regulates multiple aspects of innate immune functions and serves as a critical mediator of inflammatory responses. AIM2 inflammasome activation leads to the production of pro-inflammatory cytokines, IL-1β and IL-18 and participates triggering a pyroptosis response needed to counteract excessive cell proliferation. In addition, AIM2 expression and activation is wide regulated since alteration in its activity may derived in pathological consequences. Consequently, deregulated AIM2 activation contributes to the pathogenic processes of various inflammatory diseases. In this review, we will discuss the activation and function of AIM2 inflammasome, as well as its contribution in rheumatoid arthritis and systemic lupus erythematous pathology. Finally, we highlight the participation of the AIM2-inflammasome at the level of joint in rheumatoid arthritis and at kidney in systemic lupus erythematous. The development of therapeutic strategies based on modulation of AIM2-inflammasome activity should have a tissue-specific focus.</p>","PeriodicalId":8688,"journal":{"name":"Autoimmunity","volume":"55 7","pages":"443-454"},"PeriodicalIF":3.5,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40624513","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":"Knockdown of circ_0025908 inhibits proliferation, migration, invasion, and inflammation while stimulates apoptosis in fibroblast-like synoviocytes by regulating miR-650-dependent SCUBE2.","authors":"Ronghua Wang,&nbsp;Hongbo Li,&nbsp;Yunning Han,&nbsp;Lei Li","doi":"10.1080/08916934.2022.2102164","DOIUrl":"https://doi.org/10.1080/08916934.2022.2102164","url":null,"abstract":"<p><strong>Background: </strong>Circular RNAs (circRNAs) are demonstrated to play vital roles in human diseases, including rheumatoid arthritis (RA). Therefore, this research aimed to explore the effects of hsa_circRNA_0025908 (circ_0025908) on RA.</p><p><strong>Methods: </strong>RNA expression of circ_0025908, microRNA-650 (miR-650), and Signal peptide-CUBepidermal growth factor-like containing protein 2 (SCUBE2) were assessed by real-time quantitative polymerase chain reaction; protein expression of SCUBE2, apoptosis- and invasion-related proteins was evaluated by western blot assay. Functional assays were performed using 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl-2H-tetrazol-3-ium bromide, 5-ethynyl-2'-deoxyuridine, transwell, flow cytometry, and enzyme linked immunosorbent assay assays. Dual-luciferase reporter, RNA immunoprecipitation, and RNA pull-down assays confirmed the interaction relationship among circ_0025908, miR-650, and SCUBE2.</p><p><strong>Results: </strong>Circ_0025908 was overexpressed in synovial tissues and fibroblast-like synoviocytes (FLS) from RA patients. Inhibition of circ_0025908 repressed proliferation, migration, invasion, inflammation, and cell cycle progression, while induced apoptosis in the FLS isolated from RA patients (FLS-RA), accompanied with increased Bax, cleaved caspase-3 and E-cadherin, but declined Bcl-2, N-cadherin and Vimentin. MiR-650 was a target of circ_0025908, and SCUBE2 was a target for miR-650. Silencing of miR-650 could overturned above effects of circ_0025908 knockdown in FLS-RA, whereas its overexpression could mimic those effects by downregulating SCUBE2. Additionally, SCUBE2 expression could be positively regulated by circ_0025908 and inversely regulated by miR-650. Notably, Pearson's correlation analysis confirmed the linear correlation among circ_0025908, miR-650 and SCUBE2 in these RA tissues.</p><p><strong>Conclusion: </strong>Circ_0025908 inhibition can suppress FLS-RA dysfunctions through targeting miR-650/SCUBE2 axis, suggesting a new potential therapeutic clue for RA patients.</p>","PeriodicalId":8688,"journal":{"name":"Autoimmunity","volume":"55 7","pages":"473-484"},"PeriodicalIF":3.5,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40654675","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":"Berberine inhibits the development of endometrial cancer through circ_ZNF608/miR-377-3p/COX2 axis.","authors":"Huan Liang,&nbsp;Yi Liu,&nbsp;Lian Fu,&nbsp;Ling Li,&nbsp;Nianjin Gong","doi":"10.1080/08916934.2021.2010050","DOIUrl":"https://doi.org/10.1080/08916934.2021.2010050","url":null,"abstract":"<p><strong>Objective: </strong>Endometrial carcinoma (EC) is a common malignant tumour in women. Berberin (BBR) is an alkaloid with anti-tumour activity, and circular RNA (circRNAs) has been extensively studied in cancers. However, whether BBR regulates the development of EC by regulating circular RNA zinc finger protein 608 (ZNF608) is unknown.</p><p><strong>Methods: </strong>Different concentrations of BBR were used to treat endometrial cancer cells. A quantitative real-time polymerase chain reaction (qRT-PCR) was conducted to assess the expression of circ_ZNF608, microRNA-377-3p (miR-377-3p) and cyclooxygenase 2 (COX2). The expression of COX2 protein was detected by western blot. The effect of circ_ZNF608 in BBR-treated EC cells was verified by 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay, thymidine analog 5-ethynyl-2'-deoxyuridine (EdU) assay, colony formation assay, transwell, and flow cytometry. The effect of BBR and circ_ZNF608 on tumour growth was evaluated by xenograft tumour model <i>in vivo</i>.</p><p><strong>Results: </strong>Berberine can inhibit the proliferation and metastasis of EC cells and promote apoptosis, which is related to the concentration. Circ_ZNF608 and COX2 were abnormally increased, while the levels of miR-377-3p were reversed in EC tissues and cells. Overexpression of circ_ZNF608 can restore the inhibitory effect of BBR on EC cells. In addition, circ_ZNF608 restored the inhibitory effect of BBR on EC cells by inhibiting the expression of miR-377-3p. Similarly, MiR-377-3p/COX2 can regulate the tumour progression of EC under BBR. Finally, BBR can inhibit the growth of endometrial carcinoma <i>in vivo</i>.</p><p><strong>Conclusion: </strong>BBR was found to inhibit EC <i>via</i> the circ_ZNF608/miR-377-3p/COX2 axis, which is helpful in endometrial carcinoma.</p>","PeriodicalId":8688,"journal":{"name":"Autoimmunity","volume":"55 7","pages":"485-495"},"PeriodicalIF":3.5,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40621489","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":"MiR-300 promotes the proliferation, migration and invasion of fibroblast-like synoviocytes in rheumatoid arthritis by targeting IL-37","authors":"Ying Wang, Ge Zhang, Wei Huang","doi":"10.1080/08916934.2022.2081842","DOIUrl":"https://doi.org/10.1080/08916934.2022.2081842","url":null,"abstract":"Abstract Background Fibroblast-like synoviocytes (FLS) are crucial regulators in the pathogenesis of rheumatoid arthritis (RA). Reportedly, microRNA (miR) participates in regulating the pathogenesis of RA. In this study, we explored the regulatory effects of miR-300 on the proliferation, migration and invasion of FLS, which were obtained from RA patients. Methods qPCR was utilized to detect miR-300 expression and interleukin-37 (IL-37) mRNA expression in the synovial tissue of RA patients and healthy controls. Cell counting kit-8 (CCK-8) assay and Transwell assay were performed to investigate the regulatory function of miR-300 on the proliferation, migration and invasion of FLS. ELISA was employed to detect TNF-α, IL-6 and IL-8 levels, to evaluate the inflammatory response. Bioinformatics analysis and luciferase reporter assay were applied to validate the targeting relationship between miR-300 and IL-37. Western blot assay was executed to detect IL-37 protein expression in FLS. Results MiR-300 was revealed to be markedly down-modulated in the synovial tissue and FLS of RA patients; meanwhile, IL-37 expression was up-modulated. The transfection of miR-300 mimics enhanced RA-FLS growth, migration, invasion and inflammatory response; transfection of miR-300 inhibitors repressed the growth, migration, invasion and inflammatory response of RA-FLS. IL-37 was identified as a downstream target of miR-300, and IL-37 partially counteracted the enhanced growth, migration, invasion and inflammatory response of RA-FLS induced by miR-300. Conclusion MiR-300 facilitates growth, migration, invasion and inflammatory response of FLS by targeting IL-37, suggesting it was a crucial regulator in the pathogenesis of RA.","PeriodicalId":8688,"journal":{"name":"Autoimmunity","volume":"55 1","pages":"371 - 377"},"PeriodicalIF":3.5,"publicationDate":"2022-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46498225","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":"BML-111 alleviates inflammatory response of alveolar epithelial cells via miR-494/Slit2/Robo4 signalling axis to improve acute lung injury","authors":"F. Zou, Zhong-Bao Zhuang, Shuang-Shuang Zou, Bu Wang, Zhihua Zhang","doi":"10.1080/08916934.2022.2065671","DOIUrl":"https://doi.org/10.1080/08916934.2022.2065671","url":null,"abstract":"Abstract Acute lung injury (ALI) is a common, variously induced lung cell injury with high mortality. It is also an early stage of acute respiratory distress syndrome. BML-111 is a lipoxin A4 receptor agonist that plays an important role in inflammation. However, its function on ALI remains unclear. To explore whether BML-111 is involved in ALI and its regulatory molecular mechanism, we constructed an in vitro ALI model by stimulating primary mouse alveolar epithelial cells (AECs) with lipopolysaccharide (LPS). The downstream target of microRNA (miR)-494 was predicted by Targetscan. The apoptosis and expression of inflammatory cytokines were analysed by RT-qPCR, Western blot, and ELISA. BML-111 treatment alleviated LPS-induced apoptosis and the production of inflammatory cytokines, such as tumour necrosis factor α, interleukin (IL)-6, IL-1β, in primary mouse AECs via downregulating miR-494. MiR-494 targeted and downregulated slit guidance ligand 2 (Slit2) in primary mouse AECs. BML-111 activated the Slit2/roundabout guidance receptor 4 (Robo4) axis via downregulating miR-494 to reduce LPS-induced damage in AECs. This study elucidated that miR-494 on BML-111 alleviated LPS-induced ALI in primary mouse AECs via downregulating miR-494 and subsequently activating the Slit2/Robo4 axis. These findings provided a new idea for the prevention and treatment of ALI and respiratory distress syndrome.","PeriodicalId":8688,"journal":{"name":"Autoimmunity","volume":"55 1","pages":"318 - 327"},"PeriodicalIF":3.5,"publicationDate":"2022-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47677418","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_0060531 knockdown ameliorates IL-22-induced keratinocyte damage by binding to miR-330-5p to decrease GAB1 expression.","authors":"Quan Shi, Jing Luo, Weiming Chen, Qi He, Jianwen Long, Bo Zhang","doi":"10.1080/08916934.2022.2037127","DOIUrl":"10.1080/08916934.2022.2037127","url":null,"abstract":"<p><strong>Background: </strong>Psoriasis is a chronic immune-mediated skin disease. Recent studies showed its pathogenesis involved circular RNA (circRNA). However, the role of circ_0060531 in psoriasis development and the behind mechanism remain to be explored.</p><p><strong>Methods: </strong>Psoriasis cell model was constructed by treating keratinocytes (HaCaT cells) using interleukin 22 (IL-22). Expression of circ_0060531, microRNA-330-5p (miR-330-5p) and GRB2 associated binder 1 (GAB1) was determined by quantitative real-time polymerase chain reaction. The functional effects of circ_0060531 on IL-22-caused cell injury were investigated by 3-(4,5-Dimethylthazol-2-yl)-2,5-diphenyltetrazolium bromide, 5-Ethynyl-29-deoxyuridine, wound-healing and enzyme-linked immunosorbent assays. Protein expression was analysed by Western blot. The interactions among circ_0060531, miR-330-5p and GAB1 were identified by dual-luciferase reporter or RNA immunoprecipitation assay.</p><p><strong>Results: </strong>Circ_0060531 and GAB1 expression were significantly increased, while miR-330-5p was decreased in psoriatic skin biopsies and IL-22-stimulated HaCaT cells in comparison with controls. In function, circ_0060531 knockdown assuaged IL-22-induced cell proliferation, cell migration and inflammation. Besides, circ_0060531 acted as a miR-330-5p sponge, and regulated the processes of IL-22-treated HaCaT cells by binding to the miRNA. Under the treatment of IL-22, miR-330-5p mediated HaCaT cell damage by targeting GAB1. Importantly, circ_0060531 modulated GAB1 production by interacting with miR-330-5p.</p><p><strong>Conclusion: </strong>Circ_0060531 knockdown assuaged IL-22-induced keratinocyte dysfunction through miR-330-5p/GAB1 pathway, proving a novel target for the therapy of psoriasis.</p>","PeriodicalId":8688,"journal":{"name":"Autoimmunity","volume":"55 1","pages":"243-253"},"PeriodicalIF":3.5,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44034553","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}