Expression of several long noncoding RNAs in peripheral blood mononuclear cells of patients with systemic lupus erythematosus.

PURPOSE: Accumulating evidence has linked long noncoding RNAs (lncRNAs) to autoimmune and inflammatory disorders. This study aimed to detect the expression levels of five lncRNAs (lnc0640, lnc3643, lnc5150, lnc7514 and lncagf) in peripheral blood mononuclear cells (PBMCs) of patients with systemic lupus erythematosus (SLE), as well as their correlation with clinical and laboratory features. MATERIALS/METHODS: We recruited 76 patients with SLE and 71 normal controls into the present study, and obtained PBMCs from the blood samples of all study subjects. Expression levels of lncRNAs were determined by quantitative real-time reverse transcription polymerase chain reaction and their associations with clinical and laboratory characteristics were analyzed. RESULTS: Lnc5150 expression levels were statistically significantly decreased (Z=-6.016, P < 0.001) compared with normal controls. Lnc3643 levels were also statistically significantly decreased in SLE patients with proteinuria compared with those without (Z=-2.934, P = 0.003), and the lnc7514 levels were statistically significantly lower in anti-dsDNA(+) patients compared with anti-dsDNA(-) patients. The expression levels of lnc3643 were correlated with C-reactive protein and erythrocyte sedimentation rate (ESR), lnc7514 was correlated with disease activity and ESR (all P < 0.01). CONCLUSIONS: The aberrant lncRNA expression levels and their associations with laboratory features in SLE suggest their important role in SLE pathogenesis.

Differentially expressed circular RNAs in systemic lupus erythematosus and their clinical significance.

It has been reported that circRNAs are diff ;erentially expressed in many diseases and can be used as new biomarker to facilitate disease diagnosis. Circular RNAs (circRNAs) microarray were used to identify dysregulated circRNAs in plasma of systemic lupus erythematosus (SLE) patients. Then, we confirmed the microarray data by quantitative reverse transcription polymerase chain reaction (qRT-PCR) in both plasma and peripheral blood mononuclear cells (PBMCs) of SLE. One hundred and twelve circRNAs were identified to dysregulated expressed in plasma of SLE as compared to healthy controls. The results of qRT-PCR showed that the levels of hsa_circRNA_407176 and hsa_circRNA_001308 were decreased in both plasma and PBMCs of SLE when compared with healthy controls. The receiver operating characteristic (ROC) curve area of hsa_circRNA_407176 and hsa_circRNA_001308 in plasma were 0.599 and 0.662, respectively. The area under the ROC curves of hsa_circRNA_407176, hsa_circRNA_406567 and hsa_circRNA_001308 in PBMCs were 0.806, 0.744, and 0.722, respectively. Our study illustrated that hsa_circRNA_407176 and hsa_circRNA_001308 in plasma and PBMCs could be potential biomarkers for SLE.

RNAi Silencing of HIF-1α Ameliorates Lupus Development in MRL/lpr Mice.

Th17 cell and IL-17-mediated autoimmunity and inflammatory responses have been implicated in the development of organ damage in systemic lupus erythematosus (SLE), and new evidence suggests that hypoxia-inducible factor 1α (HIF-1α) enhances Th17 differentiation and promotes IL-17 production. However, the role of HIF-1α in the pathogenesis of lupus has not been examined. In this study, we silenced HIF-1α in vivo in a murine model of SLE to investigate whether lupus progression and the associated inflammatory pathways were affected by downregulating HIF-1α. Treatment with HIF1α-shRNA suppressed serum IL-17 level in MRL/lpr mice. Decreased anti-nucleosome antibody level, reduced urinary protein concentrations, ameliorated pathological damage, and remarkably reduced renal IgG and C3 depositions were observed in HIF1α-shRNA-treated group compared to those in the controls. Our results provide the first evidence for a role of HIF-1α in the pathogenesis of lupus and suggest a potential new therapeutic avenue for the treatment of lupus patients through reducing the HIF-1α level.

Circular RNA expression profile and potential function of hsa_circ_0045272 in systemic lupus erythematosus.

Circular RNAs (circRNAs) represent a class of non-coding RNAs that form covalently closed RNA circles with extensive expression and conservation in mammals. Circular RNAs regulate gene expression through acting as competitive endogenous RNAs (ceRNAs) and modulating gene transcription. Accumulating evidence supports the implication of circRNAs in a variety of human diseases, but studies of circRNA role in systemic lupus erythematosus (SLE) are lacking. The present study measured the circRNA expression profiles in T cells from patients with SLE and healthy controls with human circRNA microarray and identified 127 differentially expressed circRNAs in SLE patients. Down-regulation of hsa_circ_0045272 in SLE T cells was verified with quantitative PCR. Jurkat cells with stable hsa_circ_0045272 knockdown were generated using specific lentiviral short hairpin RNA for functional studies. Flow cytometric analysis indicated that hsa_circ_0045272 knockdown significantly up-regulated the early apoptosis of Jurkat cells. Meanwhile, ELISA showed that hsa_circ_0045272 knockdown significantly enhanced interleukin-2 production of activated Jurkat cells. Then, ceRNAs were predicted for hsa_circ_0045272 and the significant down-regulation of two mRNAs predicted as ceRNAs, NM_003466 (PAX8) and NM_015177 (DTX4), but not their corresponding proteins, was validated. Furthermore, dual luciferase reporter assay indicated binding of hsa_circ_0045272 with hsa-miR-6127. Circular RNA-mRNA co-expression networks showed the correlation of circRNAs with mRNAs and provided additional clues to circRNA functions. Our study demonstrated dysregulated circRNAs in SLE and revealed the function of hsa_circ_0045272 in negatively regulating apoptosis and interleukin-2 secretion and its potential mechanism. The implication of hsa_circ_0045272 and other abnormal circRNAs in SLE merits further investigation.

Potential link between m6A modification and systemic lupus erythematosus.

The field of m6A modification and epitranscriptomics has recently attracted much attention. More methods allowing for precise m6A site profiling and location are developed and crucial players of m6A modification machinery are increasingly identified. Although some challenges remain, m6A modification is found to modulate almost all aspects of RNA metabolism, such as splicing, stability, structure, translation, and export. Thus, m6A modification adds a new layer of post-transcriptional gene expression regulation, and it is implicated in T cell response to HIV infection, type I interferon production, and T cell differentiation and homeostasis. Moreover, evidence supporting its involvement in various human diseases including cancers is accumulating. Given the role of m6A modification in gene expression regulation and immune response, it invites the speculation that m6A modification may justify the pathogenesis of systemic lupus erythematosus (SLE) and take part in the initiation and progression of SLE. In this review, we introduce the widespread existence of m6A modification and briefly discuss components of m6A modification machinery in mammals. We mainly summarize the studies reporting the mechanisms of m6A modification in gene expression regulation through modulating pre-mRNA splicing, mRNA stability, RNA structure, translation, and pri-miRNA processing. Biological functions related to immune response of m6A modification and the implication of m6A modification in cancers are highlighted. In the end, we surmise the potential link between m6A modification and SLE.

Association of long noncoding RNAs expression levels and their gene polymorphisms with systemic lupus erythematosus.

Increasing evidence has demonstrated the association between long noncoding RNAs (lncRNAs) and multiple autoimmune diseases. To explore four lncRNAs (GAS5, lnc-DC, linc0597 and linc0949) expression levels and gene polymorphisms in systemic lupus erythematosus (SLE), a two stage design was applied. In the first stage, 85 SLE patients and 71 healthy controls were enrolled to investigate the lncRNAs expression levels. Then, 1260 SLE patients and 1231 healthy controls were included to detect the single nucleotide polymorphisms (SNPs) in the differentially expressed lncRNAs identified in the first stage. Linc0597, lnc-DC and GAS5 expression levels were significantly lower in SLE patients than healthy controls (P < 0.001, P < 0.001, P = 0.003 respectively). Association of five SNPs (rs10515177, rs2070107, rs2632516, rs2877877, rs2067079) with SLE risk were analyzed. No significant association was observed between these gene polymorphisms and susceptibility to SLE (all P > 0.010), and we did not find significant association between any genotypes at five SNPs and their respective lncRNAs expression in SLE (all P > 0.010). In summary, the expression levels of linc0597, lnc-DC and GAS5 are decreased in SLE patients, but their gene polymorphisms are not associated with SLE risk, and do not influence their expression levels.

Translation of noncoding RNAs: Focus on lncRNAs, pri-miRNAs, and circRNAs.

Mammalian genome is pervasively transcribed, producing large number of noncoding RNAs (ncRNAs), including long noncoding RNAs (lncRNAs), primary miRNAs (pri-miRNA), and circular RNAs (circRNAs). The translation of these ncRNAs has long been overlooked. Increasing studies, however, based on ribosome profiling in various organisms provide important clues to unanticipated translation potential of lncRNAs. Moreover, a few functional peptides encoded by lncRNAs and pri-miRNAs underline the significance of their translation. Recently, several novel researches also evidence the translation of endogenous circRNAs. Given the functional significance exemplified by peptides translated by some ncRNAs and their pervasive translation, it is not too far-fetched to image that abnormal translation of ncRNAs may contribute to human diseases. Through challenging, deciphering ncRNA translation is required for comprehensive understanding of biology and medicine. In this review, we firstly present evidence concerning translation potential of lncRNAs and go on to introduce a few functional short peptides encoded by lncRNAs. Then, salient observations showing translation of pri-miRNAs and circRNAs are described in detail. We end by discussing the impact of ncRNA translation beyond producing peptides and referring briefly to the potential role of abnormal ncRNA translation in human diseases.

Association between serum/plasma adiponectin levels and immune-mediated diseases: a meta-analysis.

Adiponectin plays an important role in the development of immune-mediated diseases. Currently published data regarding the relationship between serum/plasma levels of adiponectin and immune-mediated diseases are inconsistent. We therefore conducted this meta-analysis to explore the association of serum/plasma adiponectin levels with immune-mediated diseases in humans. Systematic literature search was conducted to identify all relevant studies. The study quality was assessed by the Newcastle-Ottawa scale. Pooled standard mean difference (SMD) with 95% confidence interval (CI) was calculated by random-effect model analysis. A total of 47 studies were included in our meta-analysis, including 27 studies of type 1 diabetes mellitus (T1DM), 9 studies of rheumatoid arthritis (RA), 7 studies of systemic lupus erythematosus (SLE), and 4 studies of ankylosing spondylitis (AS). The results revealed significant differences in serum/plasma levels of adiponectin between immune-mediated diseases and normal controls (SMD = 1.262, 95% CI 0.766-1.758, p < 0.001). In the subgroup analysis stratified by disease type, the serum/plasma levels of adiponectin in T1DM, RA and SLE patients were higher than those in normal control, but not in AS patients. Moreover, in the subgroup analysis stratified by gender, in both men and women group, the serum/plasma levels of adiponectin in patients with immune-mediated diseases were higher than that in the control group. Furthermore, subgroup analyses also showed that immune-mediated diseases from Asian population, Caucasian population, mean age >40 years, and BMI ≥24 kg/m2 had higher serum/plasma adiponectin levels when compared with normal controls. Collectively, this meta-analysis demonstrates that serum/plasma levels of adiponectin in T1DM, RA and SLE patients were higher than those in normal controls, but not in AS patients.

Comprehensive long non-coding RNA expression profiling reveals their potential roles in systemic lupus erythematosus.

Long non-coding RNAs can regulate gene transcription, modulate protein function, and act as competing endogenous RNA. Yet, their roles in systemic lupus erythematosus remain to be elucidated. We determined the expression profiles of lncRNAs in T cells of SLE patients and healthy controls using microarrays. Up to 1935 lncRNAs and 1977 mRNAs were differentially expressed. QRT-PCR showed downregulated uc001ykl.1 and ENST00000448942 in SLE patients. Expression of uc001ykl.1 correlated with erythrocyte sedimentation rate (ESR) and C-reactive protein, whereas ENST00000448942 level correlated with ESR and anti-Sm antibodies. Short time-series expression miner analysis revealed some lncRNAs whose expressions might correlate with disease activity of SLE patients. Coding-non-coding gene coexpression analyses showed differential lncRNAs might operate via modulating expressions of their correlated, relevant mRNAs in SLE. Differential lncRNAs might also function through their ceRNAs. Our study established that the aberrant expression profiles of lncRNAs may play a role in SLE and thus warrant further investigation.

Competitive endogenous RNA network: potential implication for systemic lupus erythematosus.

INTRODUCTION: Competitive endogenous RNA (ceRNA) hypothesis proposes that RNA transcripts, both coding and non-coding, crosstalk with and coregulate each other using microRNA response elements (MREs). CeRNA analysis tremendously expands functional information of coding and non-coding RNAs. Mounting evidence have shown that various types of RNAs, including pseudogenes, long non-coding RNAs, circular RNAs, and messenger RNAs, can function as ceRNAs in distinct physiological and pathophysiological states. Many validated ceRNA pairs participate in the initiation and progression of cancers, and systemic ceRNA network analyses revealing potential of ceRNAs in diagnosis, therapy, and prognosis of cancers have also been performed. Areas covered: This review concisely introduces ceRNA hypothesis and characteristics of ceRNA regulations. The major sections focus on representative examples of both protein coding and non-coding RNA transcripts acting as ceRNAs. CeRNA prediction programs and databases and implications of ceRNA network in cancers are then discussed. In the end, we surmise potential implications of ceRNA network for SLE. Expert opinion: The role of ceRNA network in systemic lupus erythematosus (SLE) remains undefined. We speculate that dissecting ceRNA network in SLE may help expand our comprehension of roles of transcriptome, particularly non-coding transcripts, and richen our knowledge of pathogenesis, diagnosis, and therapy of SLE.

Association of HLA-DQB1 polymorphisms with rheumatoid arthritis: a meta-analysis.

AIM: Studies investigating the association between HLA-DQB1 alleles and rheumatoid arthritis (RA) have reported conflicting results. The purpose of this study was to evaluate whether DQB1 alleles confer susceptibility to RA. DESIGN: A comprehensive literature search up to May 2016 was conducted to identify case-control studies on the association of HLA-DQB1 alleles with RA. Pooled ORs with 95% CIs were used to assess the strength of association. SETTING: The literature indicates that HLA-DQB1 is associated with susceptibility to RA. MAIN OUTCOME MEASURES: Frequencies of HLA-DQB1 alleles and phenotype in RA patients and healthy controls. RESULTS: Fifteen studies with 1250 cases and 1621 controls were included in this meta-analysis. DQB1 alleles were associated with RA susceptibility. The frequencies of DQB1*06 were lower in RA (p-value for comparability=0.007, OR 0.726,95% CI 0.576 to 0.916; p=0.004, OR 0.611,95% CI 0.438 to 0.852). The frequencies of DQB1*02 were lower in RA (p=0.044, OR 0.731,95% CI 0.597 to 0.895). A higher frequency of DQB1*04 was observed in RA (p=0.023, OR 1.604,95% CI 1.067 to 2.410). CONCLUSIONS: This meta-analysis demonstrates that DQB1*02 and DQB1*06 may be negatively associated with RA. Conversely, DQB1*04 may confer susceptibility to RA.

Circular RNAs and systemic lupus erythematosus.

Circular RNAs (circRNAs) are a large class of noncoding RNAs that form covalently closed RNA circles. The discovery of circRNAs discloses a new layer of gene regulation occurred post-transcriptionally. Identification of endogenous circRNAs benefits from the advance in high-throughput RNA sequencing and remains challenging. Many studies probing into the mechanisms of circRNAs formation occurred cotranscriptionally or posttranscriptionally emerge and conclude that canonical splicing mechanism, sequence properties, and certain regulatory factors are at play in the process. Although our knowledge on functions of circRNAs is rather limited, a few circRNAs are shown to sponge miRNA and regulate gene transcription. The clearest case is one circRNA CDR1as that serves as sponge of miR-7. Researches on circRNAs in human diseases such as cancers highlight the function and physical relevance of circRNAs. Given the implication of miRNAs in the initiation and progression of systemic lupus erythematosus (SLE) and the roles of circRNAs in sponging miRNA and gene regulation, it is appealing to speculate that circRNAs may associate with SLE and may be potential therapeutic targets for treatment of SLE. Future studies should attach more importance to the relationship between circRNAs and SLE. This review will concern identification, biogenesis, and function of circRNAs, introduce reports exploring the association of circRNAs with human diseases, and conjecture the potential roles of circRNAs in SLE.

A meta-analysis of the relationship between MYO9B gene polymorphisms and susceptibility to Crohn's disease and ulcerative colitis.

OBJECTIVE: Both Crohn's disease (CD) and ulcerative colitis (UC) have a complex etiology involving multiple genetic and environmental factors. Multiple UC and CD susceptibility genes have been identified through genome-wide association studies and subsequent meta-analyses. The aim of this meta-analysis was to clarify the impact of MYO9B gene polymorphisms on CD and UC risk. METHODS: The PubMed, Elsevier Science Direct and Embase databases were searched to identify eligible studies that were published before October 2014. Data were extracted and pooled crude odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated. RESULTS: A total of 11 studies, containing 3297 CD cases, 3903 UC cases and 8174 controls were included in this meta-analysis. Bonferroni correction results showed that rs1545620 A/C polymorphism of MYO9B gene was associated with both CD and UC susceptibility in Caucasians (OR=0.88, 95% CI=0.82∼0.95, P=0.001; OR=0.82, 95% CI=0.76∼0.89, P<0.001), but not in Chinese. rs1457092 G/T and rs2305764 C/T polymorphisms are associated with UC susceptibility (OR=0.85, 95% CI=0.79∼0.91, P<0.001; OR=0.88, 95% CI=0.83∼0.93, P<0.001), but not with CD susceptibility in Caucasians. CONCLUSIONS: This meta-analysis suggested that rs1545620 is both CD and UC susceptible locus in Caucasians; rs1457092 and rs2305764 are UC susceptible loci, but are not CD susceptible loci in Caucasians. Further studies with more sample size are needed for a definitive conclusion.

TCR-CD3ζ gene polymorphisms and expression profile in rheumatoid arthritis.

OBJECTIVES: Recent evidence has demonstrated that CD3ζ (also called CD247) play a vital role in multiple autoimmune diseases. In this study, we explored the association between CD247 gene single-nucleotide polymorphisms (SNPs) and rheumatoid arthritis (RA) in a Chinese Han population. We also evaluated the CD3ζ expression profile in peripheral blood mononuclear cells (PBMCs) from patients with RA and health controls. METHODS: Three CD247 polymorphisms (rs704853, rs1214611 and rs858554) were studied in 612 patients with RA and 848 controls in a Chinese population. Genotyping was performed using the Fluidigm 192.24 Dynamic Array™ Integrated Fluidic Circuit (IFC). For gene expression study, CD3ζ mRNA levels of 36 patients with RA and 39 healthy individuals were assessed by real-time polymerase chain reaction (RT-PCR). Data were analyzed by SPSS 11.5 software. RESULTS: A significant association between rs858554 polymorphism and RA was found under all genetic models (all p < 0.05). Moreover, we found the genotype distribution and allele frequency of rs858554 were significant associated with ACCP+ and RF+ phenotype as compare to health controls (all p < 0.05). Unfortunately, we did not detect any significant associations between rs704853, rs1214611 and RA susceptibility and autoantibody profiles (all p > 0.05). The gene expression assays showed that CD3ζ mRNA levels were downregulated in PBMCs of patients with RA when compared to healthy controls. CONCLUSIONS: Our results, the first reported for distinct Chinese populations, support a role of the CD247 gene in the susceptibility to RA. Further studies with more sample size are necessary to clarify the exact role of CD247 gene in the pathogenesis of RA.

Prevalence and associated factors of HIV infection among men who have sex with men in Hefei, China, 2013-2014: a cross-sectional study.

The objective of this study was to investigate the prevalence and influencing factors of HIV infection among men who have sex with men (MSM) in Hefei, China. A total of 578 MSM were recruited, with a mean age of 28.13 ± 6.91; 70.7% were under 30. The awareness rate was 95.4% (560/587) in the cross-sectional study. Of all the respondents, 73 (12.44%) were seropositive for HIV and 56 (9.54%) for syphilis. Multivariate analysis showed that self-reported sexually transmitted infections (STIs) (AOR = 8.02, 95% CI: 2.58-24.98, P < 0.001), received HIV testing in the past year (AOR = 0.33, 95% CI: 0.19-0.60, P < 0.001) and syphilis (AOR = 3.40, 95% CI: 1.69- 6.85, P = 0.001) were independently associated with HIV infection. It is necessary for post-test counselling to address risk among those who engage in sexual risk behaviours. More efforts are needed to enhance HIV/STI testing and treatment services in China.

Serum resistin levels in patients with rheumatoid arthritis and systemic lupus erythematosus: a meta-analysis.

The purpose of this meta-analysis was to investigate whether serum resistin level was associated with rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) by comparing serum resistin levels between RA or SLE patients and normal controls. PubMed and EMBASE databases (up to May 13, 2014) were used to search all related articles. The weighted mean differences (WMDs) with 95 % confidence interval (CI) were calculated using random-effect model analysis. The Cochrane Q test and I(2) statistic were used to test heterogeneity. To assess publication bias, the Egger's test and visual observation of a funnel plot were used. The Newcastle-Ottawa scale was used to assess the study quality. The STATA statistical software (version 11.0) was applied to deal with statistical data. A total of eight studies of RA including 620 patients and 460 healthy controls, and six studies of SLE including 559 patients and 430 healthy controls were finally included in the meta-analysis. The results revealed that the serum resistin levels in RA were significantly higher than those in normal controls (WMD = 0.767 ng/ml, 95 % CI = 0.114-1.419, P = 0.021), but there was no significant difference between SLE patients and normal controls (WMD = 2.771 ng/ml, 95 % CI = -0.521-6.063, P = 0.099). Publication bias was undetected. In conclusion, this meta-analysis indicate that serum resistin level was significantly elevated in RA patients.

Decreased UBASH3A mRNA Expression Levels in Peripheral Blood Mononuclear Cells from Patients with Systemic Lupus Erythematosus.

Increasing evidence has demonstrated the association between UBASH3A gene and multiple autoimmune diseases (ADs). The aim of our study was to explore the potential effect of UBASH3A messenger RNA (mRNA) expression and its role in the pathogenesis of systemic lupus erythematosus (SLE). UBASH3A mRNA levels were detected by real-time quantitative reverse transcription polymerase chain reaction (RT-qPCR) in total RNA, isolated from the peripheral blood mononuclear cells (PBMCs) of 32 SLE patients and 30 healthy donors with TRIzol Reagent. The expression level of UBASH3A mRNA was significantly reduced in PBMCs from SLE patients when compared with healthy controls (p = 0.002). UBASH3A mRNA expression levels in lower active SLE were significantly lower than that in inactive SLE groups (p = 0.000). There was a negative association between mRNA levels of hyper-active and lower-active SLE patients (p = 0.000). Moreover, a significant negative correlation between UBASH3A mRNA expression and the onset age of SLE patients was found (p = 0.044). A negative correlation was found between UBASH3A mRNA expression and SLEDAI (p = 0.049). Nevertheless, no significant difference was found between patients with lupus nephritis (LN) and those without LN (p = 0.392). The presence of leukopenia, positive for anti-dsDNA antibody and anti-SSB antibody were associated with UBASH3A mRNA levels in SLE patients (all p < 0.05). The dysregulation of UBASH3A mRNA levels in SLE patients and their correlations with experimental parameters suggested that UBASH3A may involve in the pathogenesis of SLE.

Association study of interleukin-19 rs2243188 polymorphism with systemic lupus erythematosus in a Chinese population.

The purpose of this study was to evaluate whether a single-nucleotide polymorphism (SNP), rs2243188 of interleukin-19 (IL-19), show significant evidence for association with SLE in a Chinese population. A total of 545 SLE patients and 613 healthy controls were collected in the present study. The genotyping of IL-19 rs2243188 polymorphism was detected by TaqMan allele discrimination assay on the 7300 real time polymorphism chain reaction system. The minor C allele of rs2243188, relative to the major A allele, appeared to have a significantly lower frequency in SLE patients (31.0%) as compared with controls (35.5%) (χ(2) = 5.19, p = 0.023). We also discovered a statistical significance in the dominant model (CC + CA versus AA: OR = 0.755, 95% CI = 0.598-0.953, p = 0.018). However, no significant difference in genotype distribution was found between SLE patients and controls (p = 0.056). Furthermore, an increased frequency of CC genotype were also detected in lupus nephritis (LN) groups as compared with non-LN groups (p = 0.024). Besides, the individuals with CC genotype had a 2.201-fold higher risk for the susceptibility to LN than those A allele carriers (AA + CA) (p = 0.006). Unfortunately, the analyses on the relationship of IL-19 rs2243188 with several clinical manifestations of SLE failed to find any significant results. In conclusion, our observations suggested the minor C allele of SNP rs2243188 might be a protective factor for SLE in a Chinese Han population. Moreover, the subgroup analysis highlighted that IL-19 rs2243188 SNP was associated with the susceptibility to LN patients.