Background:Anti-CD4 autoantibodies in people with HIV (PWH) receiving suppressive antiretroviral therapy (ART) appear to prevent CD4+ T cell reconstitution, yet the mechanisms underlying their production remain unclear. Emerging evidence implicates Staphylococcus aureus and its peptidoglycan (PGN) in autoimmunity. Methods:Plasma from 32 ART-naive PWH, 53 ART-treated PWH, and 32 HIV- negative controls was analyzed for IgG autoantibodies and markers of S. aureus translocation. Causality was examined in EcoHIV-infected mice administered PGN from S. aureus or Bacillus subtilis . PGN structure was analyzed via mass spectrometry. Results:Among 87 autoantibodies, 40% were elevated in ART-naive PWH and largely normalized by ART; however, anti-CD4 IgGs remained elevated in PWH on ART. Anti- CD4 IgG levels inversely correlated with CD4+ T cell counts in ART-treated PWH and positively with S. aureus translocation. In mice, S. aureus PGN induced anti-CD4 IgGs, reduced gut CD4+ T cells, and promoted surface IgG binding and apoptosis in CD4+ T cells. Conclusion:S. aureus and its PGN translocation may contribute to anti-CD4 autoimmunity and hinder immune recovery in ART-treated PWH, representing a potential therapeutic target.

Objectives: There is an intricate interplay between the microbiome and the immune response impacting development of normal immunity and autoimmunity. However, we do not fully understand how the microbiome affects production of natural-like and pathogenic autoantibodies. Peptidoglycan (PGN) is a component of the bacterial cell wall which is highly antigenic. PGNs from different bacteria can differ in their immune regulatory activities. Methods: C57BL/6 and MRL/lpr mice were intraperitoneally injected with saline or PGN from Staphylococcus aureus or Bacillus subtilis. Spleen anti-double-stranded DNA (dsDNA) IgG + B cells were sorted for B-cell receptor sequencing. Serum autoantibody levels and kidney damage were analyzed. Further, the association between plasma S. aureus translocation and systemic lupus erythematosus (SLE) pathogenesis was assessed in women. Results: Administration of B. subtilis PGN induced natural-like anti-dsDNA autoantibodies (e.g., IgM, short lived IgG response, and no tissue damage), whereas S. aureus PGN induced pathogenic anti-dsDNA autoantibodies (e. g., prolonged IgG production, low IgM, autoantibody-mediated kidney damage) in C57BL/6 and/or MRL/lpr mice. However, serum total IgG did not differ. S. aureus PGN induced antibodies with reduced clonality and greater hypermutation of IGHV3-74 in splenic anti-dsDNA IgG + B cells from C57BL/6 mice. Further, S. aureus PGN promoted IgG class switch recombination via toll-like receptor 2. Plasma S. aureus DNA levels were increased in women with SLE versus control women and correlated with levels of lupus-related autoantibodies and renal involvement. Conclusions: S. aureus PGN induces pathogenic autoantibody production, whereas B. subtilis PGN drives pro-duction of natural nonpathogenic autoantibodies.

Coronavirus disease (COVID-19) caused by SARS-CoV-2 virus is associated with a wide range of clinical manifestations, including autoimmune features and autoantibody production in a small subset of patients. Pre-exiting neutralizing autoantibodies against type I interferons (IFNs) are associated with COVID-19 disease severity. In this case report, plasma levels of IgG against type I interferons (IFNs) were increased specifically among the 103 autoantibodies tested following the second shot of COVID-19 vaccine BNT162b2 compared to pre-vaccination and further increased following the third shot of BNT162b2 in a healthy woman. Unlike COVID-19 mediated autoimmune responses, vaccination in this healthy woman did not induce autoantibodies against autoantigens associated with autoimmune diseases. Importantly, IFN-α-2a-induced STAT1 responses in human PBMCs in vitro were suppressed by adding plasma samples from the study subject post- but not pre-vaccination. After the second dose of vaccine, the study subject exhibited severe dermatitis for about six months and responded to treatments with Betamethasone Dipropionate Ointment and antihistamines for about one month. Immune responses to type I IFN can be double-edged swords in enhancing vaccine efficacy and immune responses to infectious diseases, as well as accelerating chronic disease pathogenesis (e.g., chronic viral infections and autoimmune diseases). This case highlights the BNT162b2-induced neutralizing anti-type I IFN autoantibody production, which may affect immune functions in a small subset of general population and patients with some chronic diseases.

Acute myeloid leukemia (AML) is one of the most common hematopoietic malignancies that has an unfavorable outcome and a high rate of relapse. Autophagy plays a vital role in the development of and therapeutic responses to leukemia. This study identifies a potential autophagy-related signature to monitor the prognoses of patients of AML. Transcriptomic profiles of AML patients (GSE37642) with the relevant clinical information were downloaded from Gene Expression Omnibus (GEO) as the training set while TCGA-AML and GSE12417 were used as validation cohorts. Univariate regression analyses and multivariate stepwise Cox regression analysis were respectively applied to identify the autophagy-related signature. The univariate Cox regression analysis identified 32 autophagy-related genes (ARGs) that were significantly associated with the overall survival (OS) of the patients, and were mainly rich in signaling pathways for autophagy, p53, AMPK, and TNF. A prognostic signature that comprised eight ARGs (BAG3, CALCOCO2, CAMKK2, CANX, DAPK1, P4HB, TSC2, and ULK1) and had good predictive capacity was established by LASSO–Cox stepwise regression analysis. High-risk patients were found to have significantly shorter OS than patients in low-risk group. The signature can be used as an independent prognostic predictor after adjusting for clinicopathological parameters, and was validated on two external AML sets. Differentially expressed genes analyzed in two groups were involved in inflammatory and immune signaling pathways. An analysis of tumor-infiltrating immune cells confirmed that high-risk patients had a strong immunosuppressive microenvironment. Potential druggable OS-related ARGs were then investigated through protein–drug interactions. This study provides a systematic analysis of ARGs and develops an OS-related prognostic predictor for AML patients. Further work is needed to verify its clinical utility and identify the underlying molecular mechanisms in AML.

OBJECTIVES:To investigate the risk factors for serious infections among hospitalized systemic lupus erythematosus (SLE) patients, and to provide the advice for preventing serious infections in SLE patients.METHODS:Information of SLE patients hospitalized from March 2017 to February 2019 at the Department of Rheumatology and Immunology, Xiangya Hospital, Central South University was obtained. The patients were assigned into a serious infection group and a non-serious infection group. The risk factors for serious infections among SLE inpatients were identified by comparison between the 2 groups and multivariate logistic regression analysis.RESULTS:There were 463 SLE inpatients in total, and 144 were in the serious infection group and 319 in the non-serious infection group. Multivariate logistic regression analysis showed that age ≥54.50 years old (OR=4.958, P<0.001), cardiovascular involvement (OR=6.287, P<0.001), hematologic involvement (OR=2.643, P=0.003), serum albumin <20 g/L (OR=2.340, P=0.036), C-reaction protein (CRP)/erythrocyte sedimentation rate (ESR)≥0.12 (OR=2.430, P=0.002), glucocorticoid dose ≥8.75 mg/d prednisone-equivalent (OR=2.465, P=0.002), and the combined use of immunosuppressive agents (OR=2.847, P=0.037) were the risk factors for serious infections in SLE inpatients.CONCLUSIONS:SLE patients with older age, cardiovascular involvement, hematologic involvement, low serum albumin are prone to suffering serious infections. Increased CRP/ESR ratio indicates serious infections in SLE inpatients. High-dose glucocorticoid and the combined use of immunosuppressive agents can increase the risk of serious infections in SLE inpatients.

Diagnostics is one of the most important bridge courses for medical students from basic to clinical. Doctor-patient communication runs through the whole process of patient diagnosis and treatment. How to improve medical students' ability of doctor-patient communication? Our teaching team has carried out continuous reform and explored the scientific effective teaching mode. Recently, through the construction of "doctor-patient communication skills" quality online course, efforts have made to build an online and offline blended learning mode, which has gradually realize the integration with diagnostics teaching, and has achieved remarkable results. It also provides a scientific practical basis for the integration of doctor-patient communication and other clinical courses, which is worthy of promotion.

Background: Specific factors correlated with hypothyroidism in systemic lupus erythematosus (SLE) patients remain unclear. Therefore, we aim to evaluate the prevalence of thyroid dysfunction in Chinese patients with SLE and the relationship between clinical hypothyroidism and SLE. Methods: We conducted a cross sectional study of the prevalence of thyroid dysfunction in 672 patients with SLE and 605 age- and sex-matched healthy controls. Demographic, clinical, and biochemical data were compared between 58 patients with SLE with hypothyroidism and 197 patients with SLE with euthyroidism. Multivariate analysis was performed using binomial logistic regression analysis. Spearman's rank correlation was used to identify an association between thyroid function and disease activity. Results: The prevalence of thyroid dysfunction was significantly higher in patients with SLE than in controls (70.7% vs 19.7%). SLE was associated with higher rates of hypothyroidism (9.6%, P <= 0.001) and euthyroid sick syndrome (49.6%, P <= 0.001) compared with control subjects. Further analyses showed that hypothyroidism in patients with SLE was associated with high blood pressure, renal disorder, high serum creatinine, high uric acid, hyperlipidaemia, low C3 and C4, positive anti-dsDNA antibodies, and high SLE disease activity index (SLEDAI) score. In multiple logistic regression models, albumin, platelet count, serum creatinine, and anti-dsDNA antibodies were associated with hypothyroidism. Finally, free tri-iodothyronine was significantly negatively correlated with SLEDAI score. Conclusions: Hypothyroidism was more prevalent in patients with SLE. There was a relationship between hypothyroidism with renal disorder and lupus activity. Albumin, platelet count, serum creatinine, and anti-dsDNA antibodies were correlated with hypothyroidism.

Background Little is known about chronic cannabis smoking-associated oral microbiome and its effects on central nervous system (CNS) functions. Results In the current study, we have analyzed the saliva microbiome in individuals who chronically smoked cannabis with cannabis use disorder and in non-smoking controls. We found that cannabis smoking in humans was associated with oral microbial dysbiosis. The most increased oral bacteria were Streptococcus and Actinomyces genus and the most decreased bacteria were Neisseria genus in chronic cannabis smokers compared to those in non-smokers. To investigate the function of cannabis use-associated microbiome, mice were orally exposured to Actinomyces. meyeri, Actinomyces. odontolyticus, or Neisseria. elongate through oral gavage twice per week for six months which mimics human conditions. Strikingly, oral exposure of Actinomyces meyeri, an oral pathobiont, but not the other two control bactreria, decreased global activity and increased β-amyloid 42 protein production in the mouse brains. Conclusions This is the first study to reveal that cannabis-associated enrichment of Actinomyces meyeri may contribute to a hallmark of neuropathology.

OBJECTIVE To observe the effect of enalapril on the apoptosis of renal tubular epithelial cells in renal interstitial fibrosis rats and to explore the mechanism of enalapril on renal interstitial fibrosis.
 Methods: Twenty-four SD male rats were randomly divided into a sham operation group, a model group and an enalapril group (n=8 in each group). The rats in the model group and the enalapril group underwent the operation of left urethral obstruction to establish the animal model of unilateral urethral obstruction (UUO). Fourteen days later after the operation, all rats were sacrificed and their obstructed kidneys were collected for HE and Masson staining to observe the pathological change of renal tissues. Terminal deoxynucleotidyl transferase-mediated (dUTP) nick end-labeling (TUNEL) staining was used to detect the apoptosis of renal tubular epithelial cells. Immunohistochemistry and Western blotting were used to detect the protein expression of Fas-associated death domain (FADD), apoptotic protease activating factor-1 (APAF-1) and C/EBP homologous protein (CHOP).
 Results: Compared with the sham operation group, the renal interstitial injury index and renal interstitial fibrosis index were significantly increased in the model group (P<0.05). Compared with the model group, the renal interstitial injury index and renal interstitial fibrosis index were both significantly decreased in the enalapril group (P<0.05). Compared with the sham group, the apoptosis rate of renal tubular epithelial cells was increased in the model group (P<0.05); compared with the model group, the apoptosis rate of renal tubular epithelial cells was significantly reduced in the enalapril group (P<0.05). The protein levels of FADD, APAF-1 and CHOP in the model group were significantly elevated than those in the sham group (all P<0.05), which were reversed in presence of enalapril (all P<0.05). 
 Conclusion: Enalapril can alleviate renal interstitial fibrosis through inhibiting apoptosis of renal tubular epithelial cells in UUO rats.

目的 调查湖南省长沙市痛风患者的危险因素特点,为痛风的临床防治提供科学依据. 方法 随机选择2017年7月-2018年10月湘雅医院风湿免疫科确诊的长沙市痛风患者102例(痛风组)及湘雅医院就诊的长沙市非痛风患者105例(对照组)为研究对象,进行问卷调查,用单因素和多因素方法分析各因素与痛风发病的相关性. 结果 痛风组、对照组的男女性别构成(男性:95.10％vs.42.86％)、年龄[(46.02±14.49)岁vs.(36.88±13.40)岁]、BMI[(24.70±0.28) kg/m2 vs.(22.95±0.46) kg/m2]、劳动强度构成(较大强度:54.90％vs.7.62％)、饮白酒史占比(52.94％vs.14.29％)、吸烟史占比(36.28％vs.15.24％)、高血压史占比(28.43％vs.8.57％)、高血脂史占比(42.16％vs.9.52％)、肾脏疾病史占比(21.57％vs.1.91％),差异有统计学意义(P＜0.05).以是否患痛风为因变量的多因素非条件logistic回归分析表明,男性(OR=6.245,95％ CI:1.647～23.669)、饮白酒史(OR=2.404,95％CI:1.231～7.039)、肾脏疾病史(OR=12.669,95％CI:1.609～99.737)、劳动强度较大(OR=4.415,95％CI:1.605～ 12.148)是痛风发病的独立危险因素. 结论 男性、高龄、BMI高、劳动强度较大、饮白酒、吸烟,以及有高血压、高血脂、肾脏疾病史者需高度警惕痛风的发生.

This study aimed to investigate the mechanism of fluorofenidone (AKF-PD) in treating renal interstitial fibrosis in rats with unilateral urinary obstruction (UUO). Thirty-two male Sprague-Dawley rats were randomly divided into sham, UUO, UUO + enalapril, and UUO + AKF-PD groups. All rats, except sham, underwent left urethral obstruction surgery to establish the animal model. Rats were sacrificed 14 days after surgery, and serum was collected for renal function examination. Kidneys were collected to observe pathological changes. Immunohistochemistry was performed to assess collagen I (Col I) protein expression, and terminal deoxynucleotidyl transferase-mediated nick end-labeling staining to observe the apoptosis of renal tubular epithelial cells. The expression of Fas-associated death domain (FADD), apoptotic protease activating factor-1 (Apaf-1), and C/EBP homologous protein (CHOP) proteins was evaluated by immunohistochemistry and western blot analysis. AKF-PD showed no significant effect on renal function in UUO rats. The pathological changes were alleviated significantly after enalapril or AKF-PD treatment, but with no significant differences between the two groups. Col I protein was overexpressed in the UUO group, which was inhibited by both enalapril and AKF-PD. The number of apoptotic renal tubular epithelial cells was much higher in the UUO group, and AKF-PD significantly inhibited epithelial cells apoptosis. The expression of FADD, Apaf-1, and CHOP proteins was significantly upregulated in the UUO group and downregulated by enalapril and AKF-PD. In conclusion, AKF-PD improved renal interstitial fibrosis by inhibiting apoptosis of renal tubular epithelial cells in rats with UUO.

OBJECTIVES:Lupus nephritis (LN) is an immune-complex mediated nephritis with complicated pathogenesis. The aims of the present study were to investigate whether inflammasomes are activated in the renal pathology of LN patients and analyse the association of inflammasome activation in different classes of LN renal tissues with the disease activity.METHODS:A total of 86 patients with renal biopsy-proven chronic kidney disease admitted in Xiangya Hospital from January 2015 to August 2018 were enrolled in the present study. Immunofluorescence analysis was applied to examine NLRP1, NLRP3 and AIM3 expression in renal tissues.RESULTS:AIM2 was mainly expressed in glomerular cells of LN class II. No obvious positive staining of AIM2 in renal tissues was found in other LN classes. NLRP1 and NLRP3 were mainly localised in tubular cells. NLRP1 was mainly expressed in tubular cells of LN class II and class IV while NLRP3 was expressed in tubular cells of LN class IV. Moreover, NLRP3 expression level was positive correlated with the activity index (AI) score in patients with LN.CONCLUSIONS:NLRP3, NLRP1 and AIM2 activation are involved in the progress of LN. NLRP3 activation has a positive correlation with the AI score of LN.

Objective To investigate the correlation between neutrophil-lymphocyte ratio (NLR) and disease activity of systemic lupus erythematosus (SLE),and the changes of NLR in different organ involvement of SLE patients.Methods A total of 155 SLE patients and 135 healthy controls from the Rheumatology Department of Xiangya Hospital were enrolled in this study from 2010 to 2018.Patients with SLE were divided into lupus nephritis group (LN group) and non-lupus nephritis group (non-LN group),serositis group and non-serositis group,according to whether they had kidney involvement or serositis.According to the SLE disease activity index 2000(SLEDAI-2000),the patients were divided into mild to moderate disease activity group (SLEDAI score ＜ 15) and severe disease activity group (SLEDAI score≥ 15).The NLR values of the above groups were compared.Spearman's correlation analysis was used to analyze the correlation between NLR and SLE patients' laboratory indexes.Multiple linear regression model was used to analyze the relationship between NLR and SLE disease activity.Receiver operating characteristic curve (ROC) was used to evaluate the value of NLR in SLE diagnosis and activity assessment.Results (1)The NLR value of SLE patients was significantly higher than that of healthy control group,and the difference was statistically significant (P ＜ 0.01).(2)The NLR value of SLE patients in the LN group was higher than that in the non-LN group,and the NLR value of SLE patients with serositis was higher than that in the group without serositis,with statistically significant differences (both P ＜ 0.05).(3)The NLR value of SLE patients in the severe disease activity group was higher than that in the mild and moderate disease activity group,and the difference was statistically significant (P ＜ 0.01).(4)NLR of SLE patients was positively correlated with CRP (rs=0.188,P=0.019),SLEDAI score (rs=0.264,P=0.001),and negatively correlated with total serum protein (rs=-0.250,P=0.002) and serum albumin (rs=-0.329,P ＜ 0.001),respectively.(5) Multiple linear regression showed that NLR was independently associated with SLE disease activity (B=0.351,95％CI 0.012-0.690,t=2.047,P=0.042).(6) According to ROC curve,the optimal cut-off value of NLR for SLE diagnosis was 2.17 (sensitivity 60.0％,specificity 83.1％,AUC=0.744),and the best cut-off value for predicting the activity of severe disease activity in SLE patients was 3.28 (sensitivity 58.5％,specificity 78.1％,AUC=0.700).Conclusion NLR is closely related to renal involvement,serositis and disease activity in SLE patients,which indicates that NLR,as a new inflammatory indicator,is of great significance for the assessment of SLE disease activity and organ involvement.

Behçet's disease is a multisystem inflammatory disorder. Cardiovascular involvement is rare but may present with various manifestations, resulting in high mortality. In this article, we report a young male who had chest pain accompanied by systemic involvement, and was diagnosed of Behçet's disease with serious pulmonary artery and coronary thrombosis by systemic check-up. Finally, the patient was successfully treated with a combination of prednisone and immunosuppressive agents instead of surgery. To our knowledge, this is the first report of concurrent coronary thrombosis and pulmonary artery thrombosis in Behçet's disease patients.

It is known that the quality of life (QOL) and psychological status of patients with systemic lupus erythematosus (SLE) are severely impaired. However, a few reports have assessed the QOL and psychological status in relatives of these patients. This study aimed to assess the QOL and psychological status in relatives of patients with SLE and their impact on patients. A total of 104 patient–relative dyads were evaluated using a 36-Item Short-Form Survey (SF-36), Patient Health Questionnaire (PHQ-9), Generalized Anxiety Disorder Scale (GAD-7), and Social Support Rating Scale (SSRS). Relatives of patients with SLE exhibited an impaired QOL compared with the general population (69.59 ± 22.78 vs 78.18 ± 15.88, P < 0.001) and suffered from depression (5.8 ± 5.4) and anxiety (5.8 ± 6.0). GAD-7 of relatives was positively correlated with GAD-7 of patients (r = 0.210, P < 0.05). Patients reported a lower global SF-36 score when their relatives had lower global SF-36 scores (50.13 ± 19.18 vs 58.44 ± 19.67, P < 0.05) and significantly higher SSRS when their relatives had lower PHQ-9 (41.9 ± 8.7 vs 36.3 ± 6.2, P < 0.01) or GAD-7 scores (42.8 ± 7.4 vs 36.7 ± 6.6, P < 0.01). The QOL and psychological status in relatives of patients with SLE were adversely impaired. Associations exist between the QOL and psychological status of relatives and patients with SLE. Therefore, both patients and their relatives should be taken into account when making management decisions.

OBJECTIVE:To analyze the trend relevant factors leading to death and their patterns over a 10-year period in inpatients with connective tissue diseases (CTDs).
 Methods: All clinical data about death in inpatients with CTDs were retrospectively reviewed between 2005 and 2014 at the Department of Rheumatology and Immunology in Xiangya Hospital of Central South University.
 Results: In the 10-year time period, the overall hospital mortality was 15.68‰. The disease itself accounted for 44.71% of the total causes of death, infection accounted for 42.94%, and comorbidities accounted for 12.35%. The constituent ratio of deaths and the average hospital mortality caused by the disease itself declined gradually year by year, and the constituent ratio of deaths caused by infection and comorbidities increased gradually year by year (P<0.05). In 2013-2014, infection was the leading cause of death, which accounted for 51.06%. The survival time for CTDs inpatients with interstitial lung disease (ILD) was shorter than that of CTDs inpatients without ILD, and even the risk of death was 1.722 times of the latter. The proportion of deaths caused by the disease itself was the highest in systemic sclerosis and systemic lupus erythematosus, that by infection was the highest in idiopathic inflammatory myopathy (IIM), and that by comorbidities was the highest in rheumatoid arthritis.
 Conclusion: The proportion of deaths and the hospital mortality in CTDs inpatients caused by the disease itself show a declining trend, while the proportion of deaths caused by infection and comorbidities increase. CTDs patients with ILD have shorter survival time and an increase in risk of death.

Objective To investigate the incidence and treatment of bone loss in rheumatic patients treated with glucocorticoid in China. Methods From November 1, 2012 to January 31, 2013, 3136 cases of rheumatic disease who had been or were taking glucocorticoid from 46 rheumatology centers nationwide were included and their clinical data, medications, as well as bone mass were investigated. Results (1) RA (1069 cases) and SLE ( 983 cases) patients accounted for the majority . Osteopenia or osteoporosis was observed in 90% of the 3136 patients, and 41. 4% patients were found to be osteoporotic. Nearly half of patients ( 44. 7% ) with a dosage of glucocorticosteroid ( equivalent to prednisone ) >7. 5 mg/d. Even those with a daily dose of glucocorticosteroid (equivalent to prednisone) ≤2. 5 mg, 58. 5% were reported to be osteoporotic. (2) There were increased risk of osteoporosis and fracture with age. In patients younger than 30 years of age, 74. 4% were reported of bone mass reduction or osteoporosis. (3) The incidence of abnormal bone mineral density in women were higher than that in men. The mean age at menopause was lower than that the average (45. 8 years) . (4) Most patients were not giv-en adequate treatment. Prophylactic anti-osteopontin therapy was never given in 32. 7% of patients, nor did 35. 6%of patients with T score <-2. 5 received prophylactic anti-osteoporosis treatment. The mostly used treatment were calcium and vitamin D, 20. 9% received calcium alone, only 4% received bisphosphonates. Conclusion The in-cidence of bone mass reduction or osteoporosis in Chinese rheumatic patients is high while most patients are not giv-en adequate treatment.

Objective To explore the clinical features and risk factors of lupus cystitis. Methods A total of 162 patients with systemic lupus erythematosus (SLE) were enrolled, among whom 27 patients with lupus cystitis. The clinical manifestations, laboratory findings and radiographic differences between the two groups were analyzed retrospectively. The clinical characteristics and the risk factors of patients with lupus cystitis were analyzed. Results The incidence of lupus cystitis was 1.3%. The main clinical manifestations were lower urinary tract symptoms, hydronephrosis and bilateral ureteral dilatation. The incidences of gastrointestinal symptoms in lupus cystitis patients were significantly higher than those in SLE patients without lupus cystitis (P< 0.05), while the incidence of lupus nephritis and proteinuria were statistically lower than those in the control group (P<0.05). The positive rate of anti-SSA antibody and the SLEDAI score in patients with lupus cystitis were lower than that in control group (P<0.05). Logistic regression analysis showed that gastrointestinal symptoms and low complement were the risk factors of lupus cystitis. Conclusions Gastrointestinal symptoms and low complement are risk factors of lupus cystitis. Anti-SSA antibody is closely related to lupus cystitis.

IgG4相关性疾病（IgG4-related disease，IgG4-RD）是一种免疫介导的炎性纤维化性疾病，主要病理学特征为受累组织中有大量 IgG4阳性浆细胞浸润、席纹状纤维化、伴或不伴有血清 IgG4水平升高。 IgG4-RD 作为一种全身性疾病，可累及胰腺、胆道、涎腺、泪腺、肺、肝脏、肾脏、淋巴结等多个器官组织[1]。其中肾脏受累时被称为IgG4相关性肾病（IgG4-related kidney disease， IgG4-RKD），主要包括 IgG4相关性肾小管肾间质肾炎（IgG4-related tubulointerstitial nephritis ，IgG4-related TIN）和继发于 IgG4相关性疾病的膜性肾病（membranous glomerulonephropathy ，MGN）。 IgG4-RKD 于2004年作为自身免疫性胰腺炎的器官外表现被国外首次报道[2]，国内研究相对较晚，2011年开始陆续出现病例报告。其发病机制尚不完全清楚，目前的研究表明IgG4-RD的发病机制与两条平行的途径有关：极化的CD4＋T 细胞活化巨噬细胞、肌成纤维细胞、成纤维细胞等固有免疫细胞，从而导致纤维化的产生；分泌IgG4的成浆细胞、浆细胞、IgG4抗体聚集起到抑制免疫负反馈的作用，但其中的具体环节有待进一步研究[3]。 IgG4-RKD 临床表现、血清学、影像学及组织病理有一定特点，早期治疗有助于阻止肾功能的进一步恶化。本文就IgG4相关性肾病的相关研究进展作一综述，以便能进一步认识该病、减少漏诊误诊。