Capsular contracture, a common complication following breast implant surgery, is driven by fibroblast-to-myofibroblast transition and excessive collagen deposition. Although bacterial biofilm and TGF-β signaling are implicated, the molecular mechanisms linking infection to fibrosis remain unclear. Using in vitro fibroblast models and in vivo rat capsular contracture assays, we combine transcriptomics, protein interaction analysis, and targeted mutagenesis to identify Spata13 as a critical mediator of TGF-β/Smad signaling. Functional assays assess collagen synthesis (hydroxyproline content), fibroblast proliferation (CCK-8), and myofibroblast markers (α-SMA). A competitive peptide (PT637) is designed to disrupt Spata13-TGFβRI binding. Staphylococcus epidermidis biofilm synergizes with silicone implants to upregulate Spata13, activates TGF-β/Smad signaling, and promotes fibroblast activation. Spata13 binds to TGF-β receptor I (TGFβRI) via Ser637, and its knockdown suppresses α-SMA expression and collagen deposition. The TGFβRI inhibitor LY2157299 attenuates fibrosis in vivo. Strikingly, PT637 disrupts the Spata13-TGFβRI interaction and reduces both fibrosis markers and capsular thickness in biofilm-challenged rats. We define Spata13 as a novel regulator of infection-associated fibrosis and demonstrate that targeted disruption of Spata13-TGFβRI binding by PT637 offers a precision therapeutic strategy for capsular contracture.

This case report describes an immunocompetent man in his 50s presenting with a 6-month history of facial ulcers caused by cutaneous emergomycosis.

AbstractBackgroundSystemic lupus erythematosus (SLE) is an autoimmune disease characterized by immune‐mediated inflammation affecting multiple organs and systems. The aim of this study was to establish and validate a pristane‐induced SLE model in C57BL/6J mice and analyze immune cell alterations.MethodsSix‐week‐old female C57BL/6J mice were randomly assigned to two groups (n = 6 per group). The pristane group received a single 0.5 mL intraperitoneal injection of pristane, whereas the control group received a single intraperitoneal injection of 0.5 mL saline. Urine samples were collected before injection and at 2, 4, and 6 months after injection to monitor urinary protein levels. Six months postinjection, the mice were euthanized, and serum, kidney, and spleen tissues were collected. Serum antinuclear antibody (ANA), double‐stranded DNA(dsDNA), and inflammatory cytokine levels (interleukin [IL]‐1β, IL‐6, tumor necrosis factor‐α) were quantified by enzyme‐linked immunosorbent assay. Histological alterations in kidney tissues were assessed using hematoxylin and eosin, periodic acid‐Schiff, Masson, and silver staining, in addition to direct immunofluorescence for immunoglobulin G and complement component 3. Flow cytometry was used to assess immune cell alterations in the spleen.ResultsFollowing the intraperitoneal injection of pristane, the mice exhibited a gradual increase in spleen size, body weight, and urinary protein levels. Serum levels of ANA, dsDNA, and inflammatory cytokines were elevated to varying degrees (p < 0.05). Histological analysis of the kidney sections revealed characteristic nephritic alterations, including glomerular swelling and lymphocyte infiltration. In the spleen, T cell numbers decreased, whereas the proportion of myeloid cells significantly increased, particularly monocytes, neutrophils, and macrophages (p < 0.05).ConclusionPristane successfully induced a SLE model in C57BL/6J mice, characterized by nephritic injury and significant alterations in immune cell populations.

Background:Abnormal cell-mediated immunoregulation plays a central role in the pathogenesis of systemic lupus erythematosus (SLE). Identifying distinct cellular subtypes and key genes is critical for understanding disease mechanisms. Methods:Peripheral blood scRNA-seq was performed on six SLE patients and six controls. The GSE82221 transcriptomic dataset was integrated with scRNA-seq data for a comprehensive analysis. Differentially expressed genes (bulk DEGs) and different immune cells (DICs) were identified from bulk RNA-seq analysis using differential expression and single-sample gene set enrichment analysis (ssGSEA). Key cell populations that showed similar differential patterns to DICs were identified from scRNA-seq data, and a second set of DEGs (single-cell DEGs) was obtained. Key genes were defined as the intersection of bulk and single-cell DEGs with an area under the ROC curve (AUC) > 0.7. Functional enrichment, single-cell expression analysis, methylation analysis, and protein-protein interaction (PPI) network construction were performed on the key genes. Results:From GSE82221, 2041 bulk DEGs and 14 DICs were identified. Memory B cells exhibited consistent differences between SLE and controls in both datasets. Nineteen single-cell DEGs were identified in memory B cells, with six key genes (MX1, IFI44L, ISG15, OAS1, IFI6, IFI27) showing AUC > 0.7. PPI analysis revealed their involvement in antiviral responses. Functional enrichment highlighted pathways such as Epstein-Barr virus infection and NK cell-mediated cytotoxicity. Methylation analysis showed distinct gene regulation patterns, and pseudotime analysis demonstrated dynamic expression of IFI44L and MX1 during B cell differentiation. Conclusion:This study integrated single-cell and bulk transcriptomic data to identify six key genes (MX1, IFI44L, ISG15, OAS1, IFI6, and IFI27) involved in SLE pathogenesis and highlighted the central role of memory B cells. Our findings offer new insights into SLE mechanisms and provide a theoretical basis for developing targeted therapeutic strategies.

Systemic lupus erythematosus (SLE) is a complex autoimmune disease characterised by chronic inflammation and immune dysregulation, with neutrophils playing a critical role in disease pathogenesis. In this study, we elucidated the involvement of the CXCL2-PI3K/AKT/NF-κB signalling axis in the abnormal activation of neutrophils in SLE using transcriptome analysis and functional experiments. Transcriptomic profiling revealed that CXCL2 expression is significantly upregulated in SLE patients, contributing to the activation of key inflammatory pathways and the expression of pro-inflammatory cytokines and chemokines. In vitro and in vivo experiments confirmed that CXCL2 promotes the transcription of inflammatory factors by activating the PI3K/AKT/NF-κB pathway, and inhibitors targeting this signalling axis effectively reduced inflammation. Furthermore, neutrophils from SLE patients exhibited a 'pre-activated' state under CXCL2 stimulation, potentially due to epigenetic or metabolic alterations. The functional relevance of CXCL2 was further validated in vivo, where knockout of CXCL2 or depletion of neutrophils reduced tissue damage and inflammatory responses. This study highlights the importance of the CXCL2-PI3K/AKT/NF-κB signalling axis in SLE and suggests that targeting CXCL2 or neutrophil-specific markers could provide novel therapeutic strategies for managing SLE. Future research should explore the heterogeneity of neutrophil subpopulations in SLE and the role of metabolic reprogramming in exacerbating inflammation, further refining potential targeted therapies.

BACKGROUND:There are no standards for evaluating skin photoaging. Dermoscopy is a non-invasive detection method that might be useful for evaluating photoaging.OBJECTIVE:To assess the correlation between the dermoscopic evaluation of photoaging and clinical and pathological evaluations.METHODS:The age, clinical evaluation (Fitzpatrick classification, Glogau Photoaging Classification, and Chung's standardized image ruler), histopathology (Masson staining and MMP-1 immunohistochemistry), and dermoscopy (Hu's and Isik's) of 40 donor skin samples were analyzed statistically, and Spearman rank correlation analysis was performed.RESULTS:There was a robust correlation between the total Hu scores and Isik dermoscopy. The correlation of dermoscopy with histopathology was higher than that of clinical evaluation methods. There is a strong correlation between telangiectases and lentigo. Xerosis, superficial wrinkle, diffuse erythema, telangiectases, and reticular pigmentation were significantly correlated with the three clinical evaluation methods. Superficial wrinkles were correlated with Masson, MMP-1, various clinical indicators, and other dermoscopic items.CONCLUSION:There is a good correlation between dermoscopy and clinical and histopathological examination. Dermoscopy might help evaluate skin photoaging.

BACKGROUND:Systemic lupus erythematosus is an immunologically dysregulated disease characterized by the presence of multiple autoantibodies. In SLE, B lymphocytes contribute to the dysregulated production of autoantibodies and cytokines. Recently, we discovered that miR-99a-3p binds to both EIF4EBP1 and NCAPG mRNA and that lowering miR-99a-3p can promote B cell autophagy in SLE by increasing EIF4EBP1 expression. However, the functions of miR-99a-3p and NCAPG in SLE have not been extensively investigated.OBJECTIVE:This work aims to evaluate the levels of miR-99a-3p and NCAPG expression in SLE B cells and to determine whether the aberrant expression of miR-99a-3p and NCAPG contributes to the pathological mechanisms in SLE.METHODS:B lymphocytes were obtained through immunomagnetic negative selection. Using RT-qPCR, miR-99a-3p and NCAPG mRNA expressions in B lymphocytes and in the BALL-1 cell line were measured. To determine the relative abundance of NCAPG, PI3K, p-PI3K, AKT, and p-AKT, we normalize them to the level of β-actin using Western blotting. Evaluation of miR-99a-3p and NCAPG's impact on cell proliferation was done utilizing CCK-8 assay. Using flow cytometry, the cell cycle and apoptosis were both measured.RESULTS:Comparing SLE B cells to healthy controls, miR-99a-3p expression was significantly downregulated. Additionally, it was observed that SLE B cells had significantly higher NCAPG mRNA expression. Blocking miR-99a-3p expression in BALL-1 cells with an antagomir elevated NCAPG expression, facilitated PI3K/AKT pathway activation, improved cell proliferation, raised the fraction of S-phase cells, and prevented cell apoptosis. The opposite effects of upregulated miR-99a-3p levels on BALL-1 cells were observed by using an agomir. Furthermore, the effect of decreased miR-99a-3p expression on cell proliferation was partially mediated by elevating NCAPG levels and activating the PI3K/AKT pathway.CONCLUSION:Our research indicates that lower miR-99a-3p expression in SLE B cells appears to boost B cell number via the NCAPG and PI3K/AKT pathways.

Photoaging is unique to the skin and is accompanied by an increased risk of tumors. To explore the transcriptomic regulatory mechanism of skin photoaging, the epidermis, and dermis of 16 healthy donors (eight exposed and eight non-exposed) were surgically excised and detected using total RNA-Seq. Weighted gene coexpression network analysis (WGCNA) identified the most relevant modules with exposure. The hub genes were identified using correlation, p-value, and enrichment analysis. The critical genes were identified using Support Vector Machine-Recursive Feature Elimination (SVM-RFE) and least absolute shrinkage and selection operator (LASSO) regression, then enriched using single-gene GSEA. A competitive endogenous RNA (ceRNA) network was constructed and validated using qRT-PCR. Compared with non-exposed sites, 430 mRNAs, 168 lncRNAs, and 136 miRNAs were differentially expressed in the exposed skin. WGCNA identified the module MEthistle and 12 intersecting genes from the 71 genes in this module. The enriched pathways were related to muscle. The critical genes were KLHL41, MYBPC2, and ERAP2. Single-gene GSEA identified the Hippo signaling pathway, basal cell carcinoma, cell adhesion molecules, and other pathways. Six miRNAs and 18 lncRNAs related to the critical genes constituted the ceRNA network and were verified using qPCR. The differential expression of KLHL41, MYBPC2, and ERAP2 at the protein level was verified using immunohistochemistry. KLHL41, MYBPC2, and ERAP2 genes are related to skin photoaging. The prediction model based on the three critical genes can indicate photoaging. These critical genes may have a role in skin photoaging by regulating cell growth, intercellular adhesion, and substance metabolism pathways.

Systemic Lupus Erythematosus (SLE) is an autoimmune sickness with unclear pathogenesis. The goal of this research was to reveal the heterogeneity of immune cells in SLE patients of Han and Zang nationality by single -cell RNA sequencing (scRNA-seq) and bioinformatics profiling.Methods: A total of 94,102 peripheral blood mononuclear cells (PBMCs) from six volunteers with SLE (3 Zang, 3 Han) and six healthy controls were first conducted through scRNA-seq analysis. The immune cell subsets in the pathogenesis of SLE were analyzed as well. Real-time quantitative PCR (RT-qPCR) was applied to confirm the results of sc-RNA seq analysis.Results: For the Tibetan samples, the ratios of Naive CD4 RPS4Y1 cells, Naive CD4 cells, Memory BC CD24 and Memory BC differed significantly between the SLE and control samples, while that of CD8 CTL MAL cells was significantly different between the two groups in Han nationality samples. Variable differentiation states of CD8 CTL MAL cells, CD8 CTL GZMK cells, and Naive CD4 cells were detected through pseudotime analysis. Moreover,-cell receptor (TCR) abundance was notably higher in Tibetan SLE specimens than that in controls, while B-cell receptor (BCR) abundance in Tibetan and Han samples was higher than in control groups.Conclusions: In summary, the immune cellular heterogeneity of SLE patients both Han and Zang nationality was explored based on various bioinformatics approaches, providing new perspectives for immunological characteristics of SLE among different ethnic groups.

目的 探索光老化皮肤和内源性老化皮肤的皮肤镜下特征.方法 于2021年1月至6月间收集光老化组(面部、手肘伸侧、小腿外侧)和内源性老化组(腋窝、腹部、腹股沟、大腿)各40例受试者的临床和皮肤镜影像资料,用Glogau光老化分级标准和Chung的标准化图像尺进行临床评价,用HU和Isik的皮肤镜评价方法进行皮肤镜评价.结果 光老化组受试者比内源性老化受试者Fitzpatrick分型肤色较深(P<0.001)、Glogau光老化分级较高(P=0.010)、Chung标准化图像尺(色素)得分较高(P<0.001).HU的皮肤镜下特征中网状色素(35％vs 65％,P=0.007)和线状血管(10％vs 30％,P=0.025)在光老化组中阳性率较高;Isik的皮肤镜下特征中光老化组雀斑(40％vs 10％,P=0.002)、弥漫性红斑(75％vs 40％,P=0.002)、毛细血管扩张(30％vs 5％,P=0.003)的阳性率较高,内源性老化组白线的阳性率较高(25％vs 5％,P=0.012).结论 皮肤镜可作为评估和鉴别皮肤光老化和内源性老化的辅助检测手段之一.

Acne is associated with depression and anxiety; however, the relationship between acne and suicide is still unclear. This study is aimed to evaluate the association between acne and suicide by conducting a meta-analysis. Studies were identified by electronic searches of the PubMed and EMBASE databases from their inception through Jan 10, 2020. Two authors separately assessed the quality and extracted data from the selected studies. When the heterogeneity was significant, we used a random-effects model to calculate overall pooled risk estimates. Five studies involving a total of 2,276,798 participants were finally included in the meta-analysis; 52,075 participants had acne. Suicide was positively associated with acne in the overall analysis (odds ratio (OR) 1.50, 95% confidence interval (95% CI): 1.09-2.06, P = .004, I-2 = 74.1%). Subgroup analyses were performed for suicidal behavior groups (P = .002, I-2 = 80.4%), suicidal ideation or thoughts groups (P = .849, I-2 = 0.0%), International Classification of Diseases version 9 (ICD-9) groups (P = .137, I-2 = 49.6%), non-ICD-9 groups (P = .950, I-2 = 0.0%), American groups (P = .311, I-2 = 2.4%), and non-American groups (P = .943, I-2 = 0.0%). Sensitivity analyses indicated flawed results. No publication bias was detected. Acne may significantly increase suicide risk. Clinicians should actively treat acne and consider suicide screening. Further international studies with high-quality analyses are needed as more data are published. Ethical approval and patient consent are not required because this study is a literature-based study.

系统性红斑狼疮(SLE)和狼疮性肾炎(LN)的发病机制尚未完全了解,目前认为多与遗传和环境因素有关.近年来,有学者开始关注肠道微生态对SLE发病机制的影响,肠道微生态的组成和菌群失调与自身抗体产生、B细胞的调控、不同辅助性T细胞(Th)群体内稳态的调节和调节性T细胞(Treg)的平衡以及不同Th17亚群的调节密切相关.肠道微生态的破坏称为生态失调,与自身免疫性疾病的发展紧密联系.该文将重点介绍遗传、表观遗传和环境因素对微生态和免疫系统影响的新发现,以及它们的变化对SLE和LN的发病机制的影响.

红斑狼疮(lupus erythematosus,LE)是一类慢性、反复发作的非器官特异性自身免疫病,其为病谱性疾病,70％～85％的患者有皮肤受累,其疾病谱的一端为皮肤型红斑狼疮(cutaneous lupus erythe-matosus,CLE),病变主要累及皮肤,另一端为系统性红斑狼疮(systemic lupus erythematosus,SLE),病变可累及多系统和多脏器,几乎全身各系统都可受累[1].

目的 探索伴有与不伴有皮疹的系统性红斑狼疮(systemic lupus erythematosus,SLE)患者预后和出现内脏受累的风险.方法 对2002年1月-2019年6月在昆明医科大学第二附属医院就诊的379例无皮疹和1075例有皮疹SLE患者的住院资料进行回顾性分析.有皮疹患者进一步分为皮疹逐渐出现组、皮疹逐渐消退组和持续性皮疹组进行亚组分析.比较各组间的临床特征、实验室指标、肾脏病理分型和死亡率有无差异.结果 1454例SLE患者中,男141例,女1313例.无皮疹患者发病年龄(34岁)明显大于有皮疹患者(27岁,P＜0.001).各组间的全因死亡率差异无统计学意义.有持续性冻疮样皮疹的患者全因死亡率比无冻疮样皮疹的患者更高(P =0.002).无皮疹组和皮疹逐渐消退纽的患者,比皮疹逐渐出现组和持续性皮疹组的患者肺部感染(P＜0.001)、胸腔积液(P=0.01)、肾脏受累(P =0.005)、胃肠道症状(P=0.02)、室性早搏(P=0.03)和贫血(P=0.03)的发生率更高.而皮疹逐渐出现组和持续性皮疹组的患者,比无皮疹组和皮疹逐渐消退组的患者光敏感(P ＜0.001)、关节炎(P=0.004)、血管炎(P ＜0.001)、冻疮(P=0.025)及自身抗体阳性的发生率更高.与有皮疹的患者(包括其亚组)相比,无皮疹的患者的肾脏病理分型更轻(P =0.004).结论 有持续性冻疮样皮疹的患者预后较差.无皮疹和皮疹逐渐消退的患者比皮疹逐渐出现和持续性皮疹的患者更容易出现内脏受累,但无皮疹的患者比有皮疹的患者及其亚组肾脏受累程度较轻.

Excessive activation of immune cells plays a key role in the pathogenesis of systemic lupus erythematosus (SLE). The regulation of immune cells by miRNAs is a research hotspot. In this study, second-generation high-throughput sequencing revealed a reduction in miR-99a-3p expression in patients with SLE; however, the specific mechanism underlying this phenomenon remains unclear. After transfection with an miR-99a-3p agomir, the proliferation of Ball-1 cells decreased and the levels of their apoptosis increased. The opposite effects were observed in cells transfected with the miR-99a-3p antagomir. Luciferase reporter assay indicated that miR-99a-3p directly targeted EIF4EBP1. Rescue experiments confirmed the proposed interaction between miR-99a-3p and EIF4EBP1. In vitro, in vivo and clinical investigations further confirmed that the miR-99a-3p agomir reduced the expression of EIF4EBP1, LC3B and LAMP-2A. In the in vivo experiments, serum levels of anti-nuclear antibodies, double-stranded DNA, IgE, IgM, IL-6, IL-10 and B lymphocyte stimulator were higher in mice from the antagomir group than those in mice from the MRL/lpr group. Furthermore, the protein and mRNA levels of EIF4EBP1, LC3B and LAMP-2A, the intensity of immunohistochemical staining of EIF4EBP1, LC3B and LAMP-2A, the urinary protein levels, and the C3 immunofluorescence deposition increased in mice from the antagomir group. The upregulation of miR-99a-3p expression protected B cells from EIF4EBP1-mediated autophagy, whilst the downregulation of miR-99a-3p expression induced autophagy via the EIF4EBP1-mediated regulation of the autophagy signalling pathway in B cells isolated from individuals with SLE. Based on these results, miR-99a-3p and EIF4EBP1 may be considered potential targets for SLE treatment.

Objective Systemic lupus erythematosus (SLE) is an autoimmune disease with complex etiology that is not yet entirely understood. We aimed to elucidate the mechanisms and therapeutic potential of microRNAs (miRNAs) in SLE in a Tibetan population. Methods Peripheral blood mononuclear cells from SLE patients (n = 5) and healthy controls (n = 5) were used for miRNA–mRNA co-sequencing to detect miRNAs related to immune abnormalities associated with SLE. Luciferase reporter assay was used to identify potential targets of candidate miRNA. The target genes were verified in miRNA-agomir/antagomir transfection assays with multiple cells lines and by expression analysis. The effects of candidate miRNA on monocyte and macrophage activation were evaluated by multiple cytokine profiling. Neutrophil extracellular traps (NETs) formation was analyzed in vitro by cell stimulation with supernatants of monocytes and macrophages transfected with candidate miRNA. The rodent MRL/lpr lupus model was used to evaluate the therapeutic effect of CXCL2Ab on SLE and the regulation effect of immune disorders. Results Integrated miRNA and mRNA expression profiling identified miRNA-4512 as a candidate miRNA involved in the regulation of neutrophil activation and chemokine-related pathways. MiR-4512 expression was significantly reduced in monocytes and macrophages from SLE patients. MiR-4512 suppressed the TLR4 pathway by targeting TLR4 and CXCL2. Decreased monocyte and macrophage miR-4512 levels led to the expression of multiple proinflammatory cytokines in vitro. Supernatants of miR-4512 antagomir-transfected monocytes and macrophages significantly promoted NETs formation (P < 0.05). Blocking of CXCL2 alleviated various pathogenic manifestations in MRL/lpr mice, including kidney damage and expression of immunological markers of SLE. Conclusions We here demonstrated the role of miR-4512 in innate immunity regulation in SLE. The effect of miR-4512 involves the regulation of monocytes, macrophages, and NETs formation by direct targeting of TLR4 and CXCL2, indicating the miR-4512-TLR4-CXCL2 axis as a potential novel therapeutic target in SLE.

目的:探讨抗Scl-70抗体与系统性硬化病(SSc)临床特征的相关性.方法:回顾性分析1990年1月-2018年2月该院142例SSc住院患者资料,包括性别、年龄、临床表现和实验室检查等.采用IBM SPSS Statistics 23.0软件对抗Scl-70抗体阳性和抗Scl-70抗体阴性SSc患者临床特征的差异进行统计分析.结果:本研究中抗Scl-70抗体阳性SSc患者72例(50.7％),抗Scl-70抗体阴性者70例(49.3％).与阴性组比较,阳性组中弥漫型SSc患者更多(70.8％vs.44.3％),SSc分类评分更高[(14.63±2.27)分vs.(11.40±2.72)分],起病至确诊间隔时间更短[12.0(18.0)个月vs.12.0(28.0)个月],更容易并发间质性肺病(ILD)(48.6％vs.20.0％),平均住院天数更短[(12.51±7.45)dvs.(17.71±17.89)d],差异均有统计学意义(P＜0.05).抗Scl-70抗体滴度越高,患者SSc分类为弥漫型SSc的可能性越大(P＜0.05),并发ILD的概率也越大(P＜0.05).抗Scl-70抗体滴度与SSc分类评分、抗核抗体(ANA)阳性率、红细胞沉降率(ESR)、C反应蛋白(CRP)、补体C4、低密度脂蛋白胆固醇(LDL-C)及血小板(PLT)值均呈正相关(P＜0.05).抗Scl-70抗体滴度与住院天数、抗核糖核蛋白(RNP)/Sm抗体、抗Ro52抗体、抗多发性肌炎硬皮病抗体(PM-Scl)、抗着丝点蛋白B(ACA)抗体、抗增殖细胞核抗原(PCNA)抗体、核小体、组蛋白、线粒体M2阳性率,白蛋白(ALB)及高密度脂蛋白胆固醇(HDL-C)值均呈负相关(P＜0.05).结论:抗Scl-70抗体与弥漫型SSc和ILD密切相关.抗Scl-70抗体阳性患者SSc分类评分更高,起病至确诊间隔时间更短及平均住院天数更短.

皮肤科医生经常会面临哺乳期妇女提出的有关哺乳期局部用药和全身性用药安全性的问题.哺乳期的安全数据,特别是关于皮肤科特有药物的数据非常有限,查找困难.本文通过回顾有关哺乳期常见皮肤病治疗药物安全性的文献,对皮肤科常用的药物在哺乳期的合理使用进行归纳总结.

To systematically evaluate the efficacy and safety of immunoadsorption (IAS) versus non-IAS for systemic lupus erythematosus (SLE) among Chinese population. A meta-analysis was performed by all the literatures germane to estimate the SLE patients treated with IAS and non-IAS from published randomized controlled trials (RCTs) from 1990 to February 2020. Mean differences (MDs), relative ratios (RRs), and 95% confidence intervals (CIs) were calculated, and the meta-analysis was conducted with Stata 12.0 software. A total of 18 RCTs involving 457 patients were included. The results of meta-analysis demonstrated that the IgG, Scr, Bun, ANA, 24-h urine protein, leptin, and TNF-α of IAS combined with a drug therapy group were lower than that of non-IAS, and the levels of C3 and C4 were higher than that of non-IAS after treatment in terms of laboratory parameters. In terms of adverse reactions, the incidence of fever or chills, low blood pressure, or bleeding risk was higher in the treatment group. However, there was no difference in the incidence of puncture point bleeding, thrombocytopenia, mild rash, death due to severe infection, tightness, palpitation, or chest tightness between the two groups. However, most of the adverse effects could be considered as tolerable after timely treatment. Our results indicate that IAS may be superior to non-IAS in treating SLE patients. However, due to the lower quality of included studies, high quality of multicenter, large sample size, randomized, and double-blind controlled trials are needed to validate the results.