Chi Chiu Mok, Ho So, Laniyati Hamijoyo, Nuntana Kasitanon, Der Yuan Chen, Sang Cheol Bae, Meng Tao Li, Sandra Navarra, Desmond Yat Hin Yap, Yoshiya Tanaka
The APLAR has published a set of recommendations on the management of systemic lupus erythematosus (SLE) in 2021. The current consensus paper supplements and updates specifically the treatment of lupus nephritis (LN) according to two rounds of Delphi exercise from members of the APLAR SLE special interest group, invited nephrologists, histopathologists, and lupus nephritis patients. For initial treatment of LN, we recommend a combination of glucocorticoids (GCs) with cyclophosphamide (CYC), mycophenolate mofetil (MMF), or the calcineurin inhibitors (CNIs) as first-line options. An upfront combination of immunosuppressive drugs and the biological agents may be considered in patients at significant risk of disease progression and renal function deterioration. Switching or “add-on” among different immunosuppressive agents, including biological agents, may be considered for refractory disease. Subsequent/maintenance therapy of LN should continue for at least 3 years to reduce the risk of renal flares. Lower dose MMF and azathioprine are options, but MMF maintenance should follow induction by the same drug. Prednisolone or equivalent should be maintained at a dose of 5 mg/day or less. The APLAR consensus for the management of LN includes recommendations for adjunctive therapies, monitoring and treatment of LN-related co-morbidities, and renal replacement therapies. It is hoped that this consensus paper can provide an evidence-based and pragmatic approach to the management of LN, taking into account the evidence level of therapies in Asian patients, cost-effectiveness, and differences in health care resources and reimbursement policies in the Asia-Pacific region.
{"title":"The 2024 APLAR Consensus on the Management of Lupus Nephritis","authors":"Chi Chiu Mok, Ho So, Laniyati Hamijoyo, Nuntana Kasitanon, Der Yuan Chen, Sang Cheol Bae, Meng Tao Li, Sandra Navarra, Desmond Yat Hin Yap, Yoshiya Tanaka","doi":"10.1111/1756-185X.70021","DOIUrl":"10.1111/1756-185X.70021","url":null,"abstract":"<div>\u0000 \u0000 <p>The APLAR has published a set of recommendations on the management of systemic lupus erythematosus (SLE) in 2021. The current consensus paper supplements and updates specifically the treatment of lupus nephritis (LN) according to two rounds of Delphi exercise from members of the APLAR SLE special interest group, invited nephrologists, histopathologists, and lupus nephritis patients. For initial treatment of LN, we recommend a combination of glucocorticoids (GCs) with cyclophosphamide (CYC), mycophenolate mofetil (MMF), or the calcineurin inhibitors (CNIs) as first-line options. An upfront combination of immunosuppressive drugs and the biological agents may be considered in patients at significant risk of disease progression and renal function deterioration. Switching or “add-on” among different immunosuppressive agents, including biological agents, may be considered for refractory disease. Subsequent/maintenance therapy of LN should continue for at least 3 years to reduce the risk of renal flares. Lower dose MMF and azathioprine are options, but MMF maintenance should follow induction by the same drug. Prednisolone or equivalent should be maintained at a dose of 5 mg/day or less. The APLAR consensus for the management of LN includes recommendations for adjunctive therapies, monitoring and treatment of LN-related co-morbidities, and renal replacement therapies. It is hoped that this consensus paper can provide an evidence-based and pragmatic approach to the management of LN, taking into account the evidence level of therapies in Asian patients, cost-effectiveness, and differences in health care resources and reimbursement policies in the Asia-Pacific region.</p>\u0000 </div>","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"28 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142914782","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":"What Are the Effects of Spinal Cord Stimulation for People With Low Back Pain? A Cochrane Review Summary With Commentary","authors":"Soo Chin Chan, Julia Patrick Engkasan","doi":"10.1111/1756-185X.70042","DOIUrl":"10.1111/1756-185X.70042","url":null,"abstract":"","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"28 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142909720","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}
γδT cells have been implicated in the pathogenesis of autoimmune diseases. The study aims to investigate the abundance of γδT cells in MRL/lpr mice.
Methods
MRL/lpr mice were used as lupus models, while C3H/HeJ mice served as normal controls. The abundance of γδT cells in different organs was examined by flow cytometry. Plasma double-stranded DNA antibody levels, blood urea nitrogen, creatinine, and urinary protein levels were measured. Renal histopathology was observed via H&E staining. The correlations between the abundance of γδT cells and lupus manifestations were analyzed.
Results
Compared with C3H/HeJ mice, the number of γδT cells and Vγ6+γδT cell subset in the peripheral blood of MRL/lpr mice was significantly reduced. However, in the kidney, the number of γδT cells and Vγ6+γδT cell subset was significantly increased. Additionally, the number of Vγ6+γδT cells in the kidney was positively correlated with the urinary protein level. The number of IFN-γ+Vγ6+γδT cells in the kidney was positively correlated with urinary protein level.
Conclusion
In MRL/lpr mice, it is likely that peripheral γδT cells, especially the Vγ6 subset, infiltrate the kidney and secrete IFN-γ, which contributes to the development of lupus nephritis.
背景：γδT细胞参与自身免疫性疾病的发病机制。本研究旨在探讨MRL/lpr小鼠γδT细胞的丰度。方法：以MRL/lpr小鼠为狼疮模型，C3H/HeJ小鼠为正常对照组。流式细胞术检测不同脏器中γδT细胞的丰度。测定血浆双链DNA抗体水平、血尿素氮、肌酐和尿蛋白水平。H&E染色观察肾组织病理学。分析γδT细胞丰度与狼疮表现的相关性。结果：与C3H/HeJ小鼠相比，MRL/lpr小鼠外周血中γδT细胞数量和Vγ6+γδT细胞亚群数量明显减少。而在肾脏中，γδT细胞和v - γ6+γδT细胞亚群数量明显增加。肾内v - γ6+γδT细胞数量与尿蛋白水平呈正相关。肾内IFN-γ+ v -γ 6+γδT细胞数量与尿蛋白水平呈正相关。结论：MRL/lpr小鼠的外周γδT细胞，特别是Vγ6亚群浸润肾脏，分泌IFN-γ，可能参与狼疮性肾炎的发生。
{"title":"Vγ6+γδT Cells Participate in Lupus Nephritis in MRL/Lpr Mice","authors":"Yunxia Yan, Yue Zhang, Xiaojun Tang, Zhang Zhuoya, Geng Linyu, Sun Lingyun","doi":"10.1111/1756-185X.70040","DOIUrl":"10.1111/1756-185X.70040","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>γδT cells have been implicated in the pathogenesis of autoimmune diseases. The study aims to investigate the abundance of γδT cells in MRL/<i>lpr</i> mice.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>MRL/<i>lpr</i> mice were used as lupus models, while C3H/HeJ mice served as normal controls. The abundance of γδT cells in different organs was examined by flow cytometry. Plasma double-stranded DNA antibody levels, blood urea nitrogen, creatinine, and urinary protein levels were measured. Renal histopathology was observed via H&E staining. The correlations between the abundance of γδT cells and lupus manifestations were analyzed.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Compared with C3H/HeJ mice, the number of γδT cells and Vγ6<sup>+</sup>γδT cell subset in the peripheral blood of MRL/<i>lpr</i> mice was significantly reduced. However, in the kidney, the number of γδT cells and Vγ6<sup>+</sup>γδT cell subset was significantly increased. Additionally, the number of Vγ6<sup>+</sup>γδT cells in the kidney was positively correlated with the urinary protein level. The number of IFN-γ<sup>+</sup>Vγ6<sup>+</sup>γδT cells in the kidney was positively correlated with urinary protein level.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>In MRL/<i>lpr</i> mice, it is likely that peripheral γδT cells, especially the Vγ6 subset, infiltrate the kidney and secrete IFN-γ, which contributes to the development of lupus nephritis.</p>\u0000 </section>\u0000 </div>","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"28 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142909719","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}
<p>In this study, we identified significant blood gene expression trend patterns associated with specific immune cell types in early-stage differentiation in systemic sclerosis (SSc) progression. SSc is a heterogeneous autoimmune connective tissue disease, which is mainly classified as diffuse cutaneous SSc (dcSSc) and limited cutaneous SSc (lcSSc) depending on the extent of skin fibrosis [<span>1</span>]. Although SSc is a chronic immune disorder like allergic rhinitis (AR), the antigen type in SSc is a self-antigen, in contrast to a foreign antigen in AR. We previously reported blood immune gene signatures associated with immune cell frequency change and clinical symptoms after nasal allergen challenge in patients with AR, which was used to identify immune genes with significantly different trend patterns after immunotherapy [<span>2, 3</span>]. Investigating time series gene expression from peripheral blood is useful for understanding systemic immune response changes reflecting the progression or pathophysiology of the diseases [<span>2, 4</span>].</p><p>We hypothesize that trend pattern analysis of time series blood gene expression, namely regrouping gene expression clusters into simplified trend patterns (up, down, and steady) by a given ratio threshold, can provide instinctual interpretable insight to understand the pathophysiological systemic immune response that occurs during the development of the main SSc manifestations, such as fibrosis of the skin and/or inner organs. Specifically, such an analysis may provide a viewpoint to understand key immune cell frequency or activation changes at critical crossroads during the course of the disease, particularly in early immune disease progression.</p><p>To test our hypothesis, we used public data, GSE224849, which Bellocchi et al. recently registered to report a global gene expression study of patients with preclinical systemic sclerosis (PreSSc) [<span>5</span>]. PreSSc patients with the early signs of SSc were classified by the LeRoy & Medsger classification criteria—the presence of Raynaud's phenomenon plus SSc-specific autoantibodies and/or SSc-specific nailfold video-capilaroscopic change without any other sign of definite SSc and/or fibrosis [<span>1, 5</span>]. The RNA-sequencing data were generated using blood from two PreSSc patient groups with different disease progression stages at follow-up visits.</p><p>The blood samples from 33 PreSSc patients were collected at baseline and follow-up visits (4 years later). Fourteen patients developed lcSSc (Evolving-PreSSc), a severe form of SSc with skin features such as puffy fingers and/or skin fibrosis, whereas 19 patients remained stable (Stable-PreSSc) at follow-up: Evolving-PreSSc was classified at follow-up visit as the patients with definite SSc, herein lcSSc, by reaching the minimum score of 9 based on the 2013 ACR/EULAR classification criteria for SSc. Evolving-PreSSc was characterized as having mainly puffy fingers and/or partly t
{"title":"Gene Expression Trend Pattern Analysis in Peripheral Blood From Patients With Preclinical Systemic Sclerosis","authors":"Young Woong Kim, Scott J. Tebbutt, Amrit Singh","doi":"10.1111/1756-185X.70039","DOIUrl":"10.1111/1756-185X.70039","url":null,"abstract":"<p>In this study, we identified significant blood gene expression trend patterns associated with specific immune cell types in early-stage differentiation in systemic sclerosis (SSc) progression. SSc is a heterogeneous autoimmune connective tissue disease, which is mainly classified as diffuse cutaneous SSc (dcSSc) and limited cutaneous SSc (lcSSc) depending on the extent of skin fibrosis [<span>1</span>]. Although SSc is a chronic immune disorder like allergic rhinitis (AR), the antigen type in SSc is a self-antigen, in contrast to a foreign antigen in AR. We previously reported blood immune gene signatures associated with immune cell frequency change and clinical symptoms after nasal allergen challenge in patients with AR, which was used to identify immune genes with significantly different trend patterns after immunotherapy [<span>2, 3</span>]. Investigating time series gene expression from peripheral blood is useful for understanding systemic immune response changes reflecting the progression or pathophysiology of the diseases [<span>2, 4</span>].</p><p>We hypothesize that trend pattern analysis of time series blood gene expression, namely regrouping gene expression clusters into simplified trend patterns (up, down, and steady) by a given ratio threshold, can provide instinctual interpretable insight to understand the pathophysiological systemic immune response that occurs during the development of the main SSc manifestations, such as fibrosis of the skin and/or inner organs. Specifically, such an analysis may provide a viewpoint to understand key immune cell frequency or activation changes at critical crossroads during the course of the disease, particularly in early immune disease progression.</p><p>To test our hypothesis, we used public data, GSE224849, which Bellocchi et al. recently registered to report a global gene expression study of patients with preclinical systemic sclerosis (PreSSc) [<span>5</span>]. PreSSc patients with the early signs of SSc were classified by the LeRoy & Medsger classification criteria—the presence of Raynaud's phenomenon plus SSc-specific autoantibodies and/or SSc-specific nailfold video-capilaroscopic change without any other sign of definite SSc and/or fibrosis [<span>1, 5</span>]. The RNA-sequencing data were generated using blood from two PreSSc patient groups with different disease progression stages at follow-up visits.</p><p>The blood samples from 33 PreSSc patients were collected at baseline and follow-up visits (4 years later). Fourteen patients developed lcSSc (Evolving-PreSSc), a severe form of SSc with skin features such as puffy fingers and/or skin fibrosis, whereas 19 patients remained stable (Stable-PreSSc) at follow-up: Evolving-PreSSc was classified at follow-up visit as the patients with definite SSc, herein lcSSc, by reaching the minimum score of 9 based on the 2013 ACR/EULAR classification criteria for SSc. Evolving-PreSSc was characterized as having mainly puffy fingers and/or partly t","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"28 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1756-185X.70039","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142909707","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"A Short Report on Prescription Monitoring in the Therapeutic Context of Rheumatoid Arthritis at an Italian Local Health Authority","authors":"Andrea Zovi, Roberto Langella, Francesco Ferrara","doi":"10.1111/1756-185X.70045","DOIUrl":"10.1111/1756-185X.70045","url":null,"abstract":"","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"28 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142909706","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}
Urate transporter 1 (URAT1) is a well-known therapeutic target for reducing urate levels in the treatment of hyperuricemia and gout. However, current pharmacological studies have failed to evaluate the efficacy of URAT1 inhibitors in non-primate animal models. We established a human URAT1 (hURAT1) transgenic knock-in (KI) mouse model to assess uricosuric agents' effectiveness and characterize URAT1-caused pathogenesis.
Methods
We generated hURAT1 transgenic mice using CRISPR/Cas9 KI technique. mUrat1 knockout was achieved by replacing exon 1 coding sequence with a human SLC22A12 coding sequence (CDS)-pA cassette. Based on the above transgenic mice, a hyperuricemia model was further established by hypoxanthine administration.
Results
The hURAT1-KI mice successfully expressed hURAT1 protein to the apical side of the kidney proximal tubule epithelium, where native human URAT1 is localized in human kidney. Upon hypoxanthine challenge, the blood uric acid (UA) level was elevated in hURAT1-KI mice (251 μmol/L), showing an approximately 37% increase compared to wild-type (WT) mice (183.5 μmol/L). The elevated blood UA level could be alleviated by hURAT1 inhibitor benzbromarone treatment in the hURAT1-KI mice (164.2 μmol/L vs. 251 μmol/L, p < 0.05) whereas no response was observed in WT littermates (168.8 μmol/L vs. 183.5 μmol/L).
Conclusion
The hURAT1-KI hyperuricemia mouse model would be valuable for preclinical evaluation of gout treatment with urate-lowering drugs and for studying UA metabolic complexities in humans.
{"title":"hURAT1 Transgenic Mouse Model for Evaluating Targeted Urate-Lowering Agents","authors":"Weiyan Cai, Miyi Yang, Qinghe Zhao, Guohua Yi, Peihui Lin, Apeng Chen, Gejing De","doi":"10.1111/1756-185X.70034","DOIUrl":"10.1111/1756-185X.70034","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Urate transporter 1 (URAT1) is a well-known therapeutic target for reducing urate levels in the treatment of hyperuricemia and gout. However, current pharmacological studies have failed to evaluate the efficacy of URAT1 inhibitors in non-primate animal models. We established a <i>human URAT1</i> (<i>hURAT1</i>) transgenic knock-in (KI) mouse model to assess uricosuric agents' effectiveness and characterize URAT1-caused pathogenesis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We generated <i>hURAT1</i> transgenic mice using CRISPR/Cas9 KI technique. <i>mUrat1</i> knockout was achieved by replacing exon 1 coding sequence with a human <i>SLC22A12</i> coding sequence (CDS)-pA cassette. Based on the above transgenic mice, a hyperuricemia model was further established by hypoxanthine administration.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The <i>hURAT1</i>-KI mice successfully expressed hURAT1 protein to the apical side of the kidney proximal tubule epithelium, where native human URAT1 is localized in human kidney. Upon hypoxanthine challenge, the blood uric acid (UA) level was elevated in <i>hURAT1-</i>KI mice (251 μmol/L), showing an approximately 37% increase compared to wild-type (WT) mice (183.5 μmol/L). The elevated blood UA level could be alleviated by hURAT1 inhibitor benzbromarone treatment in the <i>hURAT1</i>-KI mice (164.2 μmol/L vs. 251 μmol/L, <i>p</i> < 0.05) whereas no response was observed in <i>WT</i> littermates (168.8 μmol/L vs. 183.5 μmol/L).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>The <i>hURAT1</i>-KI hyperuricemia mouse model would be valuable for preclinical evaluation of gout treatment with urate-lowering drugs and for studying UA metabolic complexities in humans.</p>\u0000 </section>\u0000 </div>","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"28 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142909709","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}
Wei Wan, Yidi Liu, Jie Gao, Sijia Yan, Dongbao Zhao
Cellular immunotherapy is an emerging therapeutic approach that aims to utilize a patient's immune cells or engineered immune cells to treat Immune-mediated rheumatic diseases, including rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and ankylosing spondylitis (AS), among others. The PubMed database was searched for 46 relevant pieces of literature. Among them, 18 articles on T-cell therapy were used to treat RA, AS, SLE, Anti-Neutrophil Cytoplasmic Antibodies (ANCA)-associated vasculitis (AAV), and systemic sclerosis (SSc). There were nine B cell depletion therapies for RA, AS, SLE, and SSc, and 15 articles on mesenchymal stem cell (MSC) therapy for RA, AS, SLE, AAV, SSc, and Sjogren's syndrome (SS). Additionally, there were four articles on Cd19-targeting Chimeric Antigen Receptor T-Cell (CART) cell therapy for SLE and SSc treatment. The most common treatments for rheumatological diseases, such as RA, SLE, and SS, include B cell depletion, MSC extracellular vesicle therapy, and CART cell targeted therapy, while the re-used therapies for rare diseases such as SSc, IgG4-RD, and AAV include extracellular stem cell vesicles and cytokines, as per the review of the aforementioned literature. CART cell targeting therapy alone is not highly effective, and the common adverse effects include hypotension and dry cough. In summary, cellular immunotherapy has emerged as a better choice for refractory rheumatic immune diseases. In the future, further clinical studies are imperative to precisely target the treatment of rheumatic disease and provide positive outcomes to a broader patient population.
{"title":"Recent advances in cellular immunotherapy for immune-mediated rheumatic diseases","authors":"Wei Wan, Yidi Liu, Jie Gao, Sijia Yan, Dongbao Zhao","doi":"10.1111/1756-185X.15385","DOIUrl":"https://doi.org/10.1111/1756-185X.15385","url":null,"abstract":"<p>Cellular immunotherapy is an emerging therapeutic approach that aims to utilize a patient's immune cells or engineered immune cells to treat Immune-mediated rheumatic diseases, including rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and ankylosing spondylitis (AS), among others. The PubMed database was searched for 46 relevant pieces of literature. Among them, 18 articles on T-cell therapy were used to treat RA, AS, SLE, Anti-Neutrophil Cytoplasmic Antibodies (ANCA)-associated vasculitis (AAV), and systemic sclerosis (SSc). There were nine B cell depletion therapies for RA, AS, SLE, and SSc, and 15 articles on mesenchymal stem cell (MSC) therapy for RA, AS, SLE, AAV, SSc, and Sjogren's syndrome (SS). Additionally, there were four articles on Cd19-targeting Chimeric Antigen Receptor T-Cell (CART) cell therapy for SLE and SSc treatment. The most common treatments for rheumatological diseases, such as RA, SLE, and SS, include B cell depletion, MSC extracellular vesicle therapy, and CART cell targeted therapy, while the re-used therapies for rare diseases such as SSc, IgG4-RD, and AAV include extracellular stem cell vesicles and cytokines, as per the review of the aforementioned literature. CART cell targeting therapy alone is not highly effective, and the common adverse effects include hypotension and dry cough. In summary, cellular immunotherapy has emerged as a better choice for refractory rheumatic immune diseases. In the future, further clinical studies are imperative to precisely target the treatment of rheumatic disease and provide positive outcomes to a broader patient population.</p>","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"28 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143120624","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}
扫码关注我们
求助内容：
应助结果提醒方式：
京公网安备 11010802042870号