Retraction Notice to: A Novel Mechanism of Doxorubicin Resistance and Tumorigenesis Mediated by MicroRNA-501-5p-Suppressed BLID.

[This retracts the article DOI: 10.1016/j.omtn.2018.06.011.].

USP37 downregulation elevates the Chemical Sensitivity of Human Breast Cancer Cells to Adriamycin.

Background: The evolution of adriamycin (ADR) resistance in the treatment of breast cancer often leads to a poor prognosis in patients. Ubiquitin-specific peptidase 37 (USP37) has been recently identified as a modulator in regulating the stemness of breast cancer cells, but its underlying mechanism remains unclear. In this study, we investigated whether USP37 knockdown could hamper the chemical resistance of MCF-7 and MCF-7/ADR cells to adriamycin and elucidated the potential mechanism. Methods: Immunohistochemistry, western blotting, and RT-qPCR assays were performed to detect the USP37 expression in MCF-7 and MCF-7/ADR cells. The efficiency of USP37 knockdown in breast cancer cells was confirmed by western blotting and RT-qPCR assays. We also performed CCK-8 assay, flow cytometry, western blotting, and TUNEL assays to evaluate cell viability and apoptosis in breast cancer cells. In vivo study was performed to detect the tumorigenicity of MCF-7/ADR cells transfected with shScramble or shUSP37#1 under adriamycin treatment. Results: Bioinformatic analysis indicated that USP37 overexpression was positively correlated with adriamycin resistance. The expression levels of USP37 in both MCF-7 and MCF-7/ADR cells increased significantly with the exposure to adriamycin in a dose-dependent manner. It was verified by the observation that USP37 downregulation elevated the inhibitory effects of adriamycin on breast cancer cells, suppressed cell proliferation caused by cell cycle arrest in G1/S transition, as well as induced apoptosis. Furthermore, in vivo study showed that knockdown of USP37 expression also decreased tumorigenicity of MCF-7/ADR cells in mice. TUNEL assay and observation of cell morphology magnified USP37 knockdown synergized with Adriamycin could elevate the apoptosis of MCF-7 and MCF-7/ADR cells. Western blotting assay illustrated that the combination of USP37 knockdown with adriamycin treatment significantly upregulated the expression levels of cleaved caspase 3 and Bax, whereas the expression level of Bcl-2 was inhibited. Conclusion: Knockdown of USP37 gene expression can reverse the resistance of breast cancer cells to adriamycin, and down-regulating USP37 might be a valuable strategy against ADR resistance in breast cancer therapy.

A Novel Mechanism of Doxorubicin Resistance and Tumorigenesis Mediated by MicroRNA-501-5p-Suppressed BLID.

Doxorubicin is a widely used anthracycline-based anti-tumor agent for both solid and liquid tumors. Mounting evidence has demonstrated that microRNAs (miRNAs) are involved in chemoresistance and tumorigenesis. However, the roles of microRNA-501-5p (miR-501) in doxorubicin resistance and gastric cancer cell proliferation and invasion are still not fully understood. In this study, we identified that BLID (BH3-like motif-containing protein, cell death inducer) was directly regulated by miR-501 at the post-transcriptional level in multiple gastric cancer cell lines. Endogenous miR-501 was higher, whereas BLID was lower, in doxorubicin-resistant gastric cancer SGC7901/ADR cells compared with their parental SGC7901 cells. miR-501 suppressed gastric cancer cell apoptosis, induced resistance to doxorubicin, and enhanced cell proliferation, migration, and invasion. Subcutaneous injection of miR-501 lentivirus-infected SGC7901 cells resulted in rapid growth of xenograft tumors and resistance to doxorubicin treatment, unlike injection of negative miRNA lentivirus-infected SGC7901 cells. This is achieved at least partially by directly targeting BLID and subsequent inactivation of caspase-9 and caspase-3 and phosphorylation of Akt. Taken together, miR-501 induces doxorubicin resistance and enhances the tumorigenesis of gastric cancer cells by suppressing BLID. miR-501 might be a potential target for doxorubicin resistance and gastric cancer therapy.

The mechanism between epithelial mesenchymal transition in breast cancer and hypoxia microenvironment.

Hypoxia microenvironment widely exists in solid tumor tissues, which is mainly due to the rapid growth of cells within the tumor more than the speed of capillary in neoplasm, resulting in tumor tissue hypoxia. In hypoxia, hypoxia inducible factor 1 (HIF-1) is activated and regulate the expression of a series of hypoxia inducible genes, resulting in a series of hypoxia adaptation reaction. Researchs proved that, HIF-1 is closely related to the invasion, metastasis, prognosis of the tumor, and the expression of HIF-1 is higher in metastatic tissues compared with primary cancer tissues. In the evolution process of breast cancer, epithelial mesenchymal transition (EMT) define the characteristics of migration and invasion of breast cancer cells, which can also allow cancer cells to acquire the ability of self-renewing and stemness, so as to promote the generation of breast cancer stem cells. The incidence of EMT cancer stem cells are higher within the resistant to conventional treatment. This review focuses on breast cancer (stem cells), targeting the mechanism between hypoxia and EMT in tumor (stem cells), with the purpose of finding the new therapy to breast cancer.

[Efficacy on analgesia with electric stimulation of long-term retaining needle after laparoscopic cholecystectomy].

OBJECTIVE: To observe the clinical effect of electric stimulation of long-term retaining needle on analgesia after laparoscopic cholecystectomy (LC) and the impacts on the post-surgical flatus time. METHODS: Under static absorptive composite general anesthesia, 90 cases of LC were randomized into three groups, 30 cases in each one. In the control group, the analgesia was not applied after LC. In the analgesia-pumper group, the patient controlled intravenous analgesia (PCIA) was used. In the needle-retaining group, the electric acupuncture stimulator was used. The needles were inserted transversely at Riyue (GB 24), Qichong (ST 30) and Yanglingquan (GB 34) and fixed with sterile sticker. Separately, in 8 h and 24 h after surgery, the electric acupuncture stimulation with disperse-dense wave, 2 Hz/100 Hz frequency was applied continuously for 30 min. Visual analogue scale (VAS), adverse reactions such as vomiting and nausea and the postoperative flatus time in 2, 4, 8, 12, 24 and 36 h after surgery were observed and recorded in the three groups. RESULTS: In 2, 4, 8, 12 and 24 h after surgery, VAS scores in the needle-retaining group and the analgesia-pumper group were all lower than those in the control group (P < 0.05, P < 0.01). The analgesia effect at the above time points in the needle-retaining group was better than that in the analgesia-pumper group (all P < 0.05). There was not adverse reaction in the needle-retaining group. But there were 3 cases of somnolence, 6 cases of nausea and 3 cases of vomiting in the analgesia-pumper group, and 2 cases of nausea and 1 case of vomiting in the control group. The flatus time was quite earlier in the needle-retaining group as compared with the other two groups [(14.77 +/- 4.99) h vs (18.50 +/- 4.22) h, P < 0.01; (14.77 +/- 4.99) h vs (18.17 +/- 4.69) h, P < 0.05]. CONCLUSION: The electric stimulation of long-term retaining needle is safe and effective in analgesia after LC. It avoids the adverse reactions of analgesics and promotes postoperative flatus.

IKKα restoration via EZH2 suppression induces nasopharyngeal carcinoma differentiation.

Lack of cellular differentiation is a key feature of nasopharyngeal carcinoma (NPC), but it also presents as a unique opportunity for intervention by differentiation therapy. Here using RNA-seq profiling analysis and functional assays, we demonstrate that reduced IKKα expression is responsible for the undifferentiated phenotype of NPC. Conversely, overexpression of IKKα induces differentiation and reduces tumorigenicity of NPC cells without activating NF-κB signalling. Importantly, we describe a mechanism whereby EZH2 directs IKKα transcriptional repression via H3K27 histone methylation on the IKKα promoter. The differentiation agent, retinoic acid, increases IKKα expression by suppressing EZH2-mediated H3K27 histone methylation, resulting in enhanced differentiation of NPC cells. In agreement, an inverse correlation between IKKα (low) and EZH2 (high) expression is associated with a lack of differentiation in NPC patient samples. Collectively, these findings demonstrate a role for IKKα in NPC differentiation and reveal an epigenetic mechanism for IKKα regulation, unveiling a new avenue for differentiation therapy.

Annexin A7 and its binding protein galectin-3 influence mouse hepatocellular carcinoma cell line in vitro.

Lymph node metastasis is recognized as an important mode of liver cancer metastasis. Our previous study has built two hepatocarcinoma cell lines, Hca-F with high (75%) and Hca-P with low (25%) incidences of lymph node metastasis, and has indicated that annexin A7 is an important factor in the lymphatic metastasis of tumors. There is evidence that galectin-3 is the binding protein of annexin A7 and works in protein complexes. Our current study shows that both annexin A7 and galectin-3 express higher in Hca-F than Hca-P. Annexin A7 was successfully down-regulated in Hca-P by RNA interference, and this resulted in concomitant reduction of galactin 3 expression in annexin A7 down regulated compared to the control and N-control cells. Using CCK-8 assay, the expression level of annexin A7 and galectin-3 were found to have correlation with the proliferation ability; Transwell assay showed annexin A7 and galectin-3 are involved in cell migration and invasion regulation in mouse hepatocellular carcinoma cell lines, immunofluorescence assay indicate annexin A7 and galectin-3 were co-located annexin A7 and galectin-3 played roles in DNA damage and cell proliferation cycle checkpoint arrest pathway. Those phenomena indicated that annexin A7 influences lymphatic metastasis of tumors by interacting with galectin-3 through the regulation of tumor cell proliferation, attachment, migration and invasion.

Decreased ITGAM and FcγRIIIA mRNA expression levels in peripheral blood mononuclear cells from patients with systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is a multisystem autoimmune disease with complex genetic predisposing factors involved. ITGAM and FCγRIIIA are two kinds of immune complex clearance molecules. The variants in ITGAM and FCγRIIIA genes have been confirmed to be associated with SLE. The aim of this study is to investigate the association of mRNA expression levels of ITGAM and FCγRIIIA with SLE. Real-time transcription-polymerase chain reaction analysis (RT-PCR) was used to determine the expression levels of ITGAM and FCγRIIIA mRNA in peripheral blood mononuclear cells (PBMC) from 60 patients with SLE and 60 healthy controls. Flow cytometry was used to measure the expression level of ITGAM and FcγRIIIA from 30 SLE patients and 30 healthy controls. The expression levels of ITGAM mRNA was significantly decreased in SLE patients compared with healthy controls (P = 0.007). Patients with arthritis had higher ITGAM mRNA level than those without arthritis (P = 0.029). The expression level of FCγRIIIA mRNA in SLE patients was significantly lower than that of healthy controls (P = 0.001). Decreased expression level of FCγRIIIA mRNA was also found in patients with LN compared with those without LN (P = 0.015). The level of ITGAM mRNA in patients with anti-SSB positive, anti-RNP positive, complement reduction and increased IgG was significantly reduced. No significant correlation was found between ITGAM and FcγRIIIA mRNA expression level in SLE patients (r = -0.019, P = 0.882). Expression of ITGAM protein in T cells, neutrophil and monocyte of SLE patients was significantly lower than healthy controls (P < 0.05). For FcγRIIIA protein expression in monocyte and NK cells, there were no significant difference between SLE patients and healthy controls (P > 0.05). The altered expression levels of ITGAM and FCγRIIIA mRNA in SLE patients and their correlations with clinical data suggest that ITGAM and FCγRIIIA may play a role in this disease.

[Down-regulation of Smoothened gene expression inhibits proliferation of breast cancer stem cells].

OBJECTIVE: To investigate the influence of down-regulating Smoothened (SMO) gene expression through short hairpin RNA (shRNA) on the proliferation of breast cancer stem cells. METHODS: Human SMO shRNA was designed, synthesized chemically, and transfected into MCF-7 cells to down-regulate SMO gene. By using G418, stable cells with down-regulated SMO were selected. In vitro proliferation of these cells was measured by CCK8 assay. The proportion of CD44(+)/CD24(-) cells was detected by flow cytometry and the mammospheres formation was determined by suspension sphere culture. The expression of SMO, GLI1 and Oct4 was detected by Western blot. In vivo, the volume of tumor was measured every 3 days and the expression of SMO, GLI1 and Oct4 detected by Western blot. RESULTS: In vitro, the cells were transfected with SMO-shRNA and selected by G418 after 21 days. SMO-shRNA effectively down-regulated the expression of SMO gene and protein, and inhibited the proliferation of MCF-7 and markedly reduced the proportion of CD44(+)/CD24(-) cells and mammospheres. In vivo, SMO-shRNA treatment of MCF-7 significantly inhibited the volume of tumor. The positive rate of SMO in negative control and SMO-shRNA group was 5/5 and 2/5, respectively. The expression of SMO, GLI1 and Oct4 in different groups were 0.72 ± 0.17 and 0.21 ± 0.09, 1.21 ± 0.21 and 0.47 ± 0.12, 0.83 ± 0.13 and 0.25 ± 0.07. SMO, GLI1 and Oct4 down-regulation significantly suppressed at protein levels (P < 0.05). CONCLUSION: The shRNA by chemical synthesis can effectively down-regulate SMO gene expression and inhibit the proliferation of breast cancer stem cells.

Evidence for H5 avian influenza infection in Zhejiang province, China, 2010-2012: a cross-sectional study.

BACKGROUND: The first outbreak of H5N1 highly-pathogenic avian influenza (HPAI) virus associated with several human deaths occurred in 1997 in Hong-Kong, China. While H5N1 virus infection in poultry workers has been studied in some detail, little is known about the environmental risk factors of the H5 avian influenza virus infection in China. METHODS: A cross-sectional study was performed to evaluate the environmental load of H5 viruses in poultry-contaminated environments and to explore potential risk factors associated with infection in poultry workers between October 2010 and March 2012. Serum and environmental samples were collected in Zhejiang province, China. The hemagglutination inhibition (HI) assay was used to analyze human sera for antibodies against H5N1 virus [A/Hubei/1/2010 (H5N1) and A/Anhui/1/2005 (H5N1)]. All participants were interviewed with a standardized questionnaire to collect information on exposure to poultry. H5 Avian influenza virus in the environmental samples was detected by real time RT-PCR. RESULTS: One hundred and five of 3,453 environmental samples (3.0%) tested positive for H5 avian influenza virus. Fifty-five of 1,169 subjects (4.7%) tested seropositive for anti-H5N1 antibodies. A statistically significant difference in H5 virus detection rate was found among the different environments sampled (<0.001), with the highest showed in live bird markets (68.6%). Detection rate varied according to the source of samples, sewage (9.5%), drinking water (19.0%), feces (19.0%), cage surface (25.7%), and slaughtering chopping boards (15.2%), respectively. Direct or close contact with poultry (OR =5.20, 95% CI, 1.53-17.74) and breeding numerous poultry (OR =3.77, 95% CI, 1.72-8.73) were significantly associated with seroprevalence of antibodies to avian influenza virus A (H5N1). CONCLUSIONS: The number of birds bred more than 1,000 and direct or close contact with poultry in the workplace or the environment would be a potential risk of H5N1 infection.

Association of BLK (rs13277113, rs2248932) polymorphism with systemic lupus erythematosus: a meta-analysis.

The B-cell lymphocyte kinase (BLK) is a src-family protein tyrosine kinase specifically expressed in B-lineage cells that has been implicated in the pathogenesis of systemic lupus erythematosus (SLE) and has been investigated in numerous ethnically diverse studies. However, genetic association studies that have examined the association between BLK gene variants and SLE have produced conflicting results. To shed further light on this issue, we performed a meta-analysis of the association between rs13277113, rs2248932 polymorphism and SLE in different ethnic groups. An updated literature-based meta-analysis of six original articles involving 20,271 control individuals and 11,796 subjects with SLE was conducted. Crude ORs with 95% CIs were used to assess the strength of association between rs13277113, rs2248932 polymorphism and SLE risk. Publication bias was estimated using Egger's linear regression test. The authors assessed the evidence of genotypic association using STATA Version 10.0. The combined overall odds ratio, calculated for SLE and the risk A-allele of rs13277113 was 1.416 (95% CI: 1.358, 1.477). An odds ratio of 1.264 (95% CI: 1.208, 1.322) was found for the T-allele of rs2248932. Significant associations of rs13277113 and SLE were observed for dominant model (AA + AG vs. GG, OR: 1.518; 95% CI: 1.411, 1.632), and recessive model (AA vs. AG + GG, OR: 1.553; 95% CI: 1.461, 1.651); so were rs2248932 and SLE for dominant model (TT + TC vs. CC, OR: 1.342; 95% CI: 1.233, 1.460), and recessive model (TT vs. TC + CC, OR: 1.338; 95% CI: 1.257, 1.424). All of these were conducted in fixed effects model as heterogeneity was not detected. Tests for bias revealed no evidence of biases. On the assessment of available evidence, the authors concluded that moderate evidence exists for an association between the BLK rs13277113, rs2248932 variants and SLE. Therefore, further research is warranted on the role of BLK polymorphisms in the etiology of SLE.

Lack of association of FcγRIIIb polymorphisms with systemic lupus erythematosus: a meta-analysis.

Systemic lupus erythematosus (SLE) is a complex autoimmune disease. Fcγ receptor genes have been suggested to play an important role in the pathogenesis of SLE and lupus nephritis (LN). This study aims to assess the association between FcγRIIIb-NA1/NA2 polymorphism and the susceptibility to SLE and lupus nephritis. Relevant studies were identified from electronic databases. A meta-analysis was performed for heterogeneity test and pooled OR calculation. The overall OR of NA2/NA2 homozygous genotype and NA2 allele frequency showed no significant association with SLE and lupus nephritis. Similarly, the association between FcγRIIIb-NA1/NA2 polymorphism and SLE and lupus nephritis was not found in European and Asian population. Taken together, our results suggest that FcγRIIIb might not be a susceptibility gene for SLE and lupus nephritis.

[Expression of chromogranin A in human mammary tissues].

OBJECTIVE: To explore the pathogenesis and significance of neuroendocrine breast carcinoma by detecting chromogranin A (CgA) in human mammary tissues. METHOD: Eighty-nine cases of human mammary tissues were collected to detect CgA expression using immunohistochemistry. RESULT: No CgA expression was detected in normal or hyperplastic tissues, but its expression was found in mammary carcinoma tissues at the rate of 16.7%. A significant difference in CgA expression was found between cancer tissues and non-cancer tissues, but not between the cancer tissues with different pathological grades. CONCLUSION: The pathogenesis of mammary neuroendocrine carcinoma may involve the micro-environmental factors that affect the differentiation of stem cells to give rise to immature cells, cell differentiation in other lineages or transdifferentiation. CgA may serve as an immunological parameter for this type of breast cancer in routine screening test.

A meta-analysis of the association of STAT4 polymorphism with systemic lupus erythematosus.

STAT4 has been newly identified as a susceptibility gene for systemic lupus erythematosus (SLE) in recent reports. To more precisely estimate the association between STAT4 polymorphism and SLE risk, a meta-analysis was performed. Studies on the association of STAT4 rs7574865 or rs7601754 with SLE were fully considered and carefully selected using three electronic databases (PubMed, Embase, and Web of Science). A total of 17 comparisons from 8 relevant studies involving 7,381 patients and 11,431 controls were included to analyze the association between STAT4 rs7574865 and SLE risk. The pooled OR for the minor T allele of STAT4 rs7574865 was 1.65 (95% CI 1.56-1.75, P < 0.001) in SLE. In a subgroup analysis by ethnicity, the degree of risk of STAT4 rs7574865 with SLE susceptibility was similar in populations of European or Asian origin, although significant differences in the minor T allele frequencies were observed in the two population controls. As for rs7601754, there were five comparisons from four relevant studies involving 2,498 patients and 4,825 controls in this meta-analysis. The pooled OR for the minor C allele of STAT4 rs7601754 was 0.67 (95% CI 0.59-0.75, P < 0.001) in SLE. Conversely, the major T allele of STAT4 rs7601754 might be a risk factor for SLE risk. In conclusion, our results do support STAT4 rs7574865 polymorphism as a susceptibility factor for SLE in populations of European and Asian origin. Our results also suggest that STAT4 rs7601754 polymorphism might be associated with SLE risk.

Increased serum interleukin 17 in patients with systemic lupus erythematosus.

Interleukin 17 (IL-17) is a Th17 cytokine associated with inflammation, autoimmunity and defense against some bacteria, it has been implicated in many chronic autoimmune diseases including psoriasis, multiple sclerosis and systemic sclerosis. However, whether IL-17 plays a role in the pathogenesis of systemic lupus erythematosus (SLE) remains unclear. In the present study, we aimed to investigate the serum IL-17 level in patients with SLE and it's associations with disease manifestations and activity. Fifty-seven patients with SLE and 30 healthy volunteers were recruited. Serum IL-17 levels were examined by enzyme linked immunosorbent assay (ELISA). Statistic analyzes were performed by SPSS 10.01. Results show that serum IL-17 levels were significantly elevated in SLE patients as compared with normal controls. Nevertheless, no associations of serum IL-17 level with clinical and laboratory parameters were found; no significant difference regarding serum IL-17 level between SLE patients with nephritis and those without nephritis was found; no significant difference was found between Less active SLE and More active SLE; Correlation analysis between serum IL-17 levels and SLEDAI showed no association. Taken together, our results indicate increased serum IL-17 levels in SLE patients, suggesting that this cytokine may trigger the inflammatory process in SLE. However, no associations of serum IL-17 level with disease manifestations were found. Therefore, further studies are required to confirm this preliminary data.

Study on clinical features and complications with systemic lupus erythematosus (SLE) activity in Chinese Han population.

Systemic lupus erythematosus (SLE) is a complex autoimmune disease affecting multiple organs/systems with variable activities. We performed a retrospective study to investigate the relationship of clinical characteristics and complications with SLE activity in Chinese Han population. A cohort of 1,490 SLE inpatients was evaluated for disease activity using the systemic lupus erythematosus disease activity index (SLEDAI). Chi-square test or Fisher's exact test was used to compare differences of clinical and laboratory features between active and inactive SLE patients. Logistic regression was chosen to explore the pattern of risk factors for disease activity. We found that neuropsychiatric involvement, nephritis, arthralgia, anti-dsDNA, serositis, hypocomplementemia, oral ulcerations, erythrocyte sedimentation rate, low C3, hematological abnormalities, and systolic pressure (1.010 < odds ratio < 10.568, 1.002 < 95% confidence interval < 31.599, 0.000 < P < 0.026) were major factors associated with disease activity, but not headaches, anti-ribonucleoprotein or anti-Sm, C-reactive protein, and anemia (P > 0.05, respectively). The involvements of urinary system, respiratory system, and central nervous system were significantly more frequent in active SLE than inactive SLE (0.000 < P < 0.014), except for alimentary system (P = 0.399). Our study has comprehensively evaluated the relationship of clinical characteristics and organs/systems involvement of SLE with SLEDAI in Chinese Han population and presented a compendium of factors affecting SLE, which should be useful for better evaluating disease activity and predicting organs/systems damage in SLE for clinical assessments and managements.

Condom use among married women at risk for sexually transmitted infections and HIV in rural China.

OBJECTIVE: To assess factors associated with condom use among married women in rural China, and provide evidence for implementing education strategies to prevent sexually transmitted infections and HIV. METHODS: A total of 737 sexually active married rural women who were aged between 18 and 49 years and had heard of AIDS were selected by cluster sampling and interviewed in 8 villages of Anhui province, China. RESULTS: The rate of condom use was only 5.4%.There were no significant differences in sexual behavior and condom use between married women whose husbands were away as migrant workers and the wives of nonmigrant men, except in knowledge of free condom sources. Significant factors associated with condom use included age, level of education, knowledge about condoms, training about condoms, sources of condoms, and husbands' attitude toward condoms. CONCLUSIONS: More educational interventions are needed to increase condom knowledge and promotion, especially among less educated women and married women left behind by migrant husbands.

The expressions of Toll-like receptor 9 and T-bet in circulating B and T cells in newly diagnosed, untreated systemic lupus erythematosus and correlations with disease activity and laboratory data in a Chinese population.

Toll-like receptor 9 (TLR9) plays a controversial role in the pathogenesis of systemic lupus erythematosus (SLE). T-bet may be involved in the processes between the initiation of TLR9 activation and the antibodies' production. To clarify the paradox of TLR9, we investigated the intracellular expressions of TLR9 and T-bet in B and T cells in peripheral blood samples from 35 newly diagnosed, untreated patients with SLE and 16 healthy subjects by flow cytometry (FCM). And we collected the clinic laboratory data obtained from the same individual blood sample tested by FCM each time. And the correlations among the expression levels of the two proteins and SLE laboratory data were calculated. We found the percentages of B cells expressing TLR9 and T-bet and of T cells expressing TLR9 were significantly elevated in SLE patients when compared with healthy controls. There was a significantly negative relationship between the proportion of B cells expressing TLR9 and SLE Disease Activity Index (SLEDAI) score. The serum levels of anti-dsDNA antibody reversely correlated with the mean fluorescence intensity (MFI) of B cells co-expressing T-bet and TLR9. The serum levels of anti-C1q antibody significantly associated with the proportion of B cells expressing T-bet. Also, the serum levels of IgM and IgA antibodies both significantly correlated with TLR9 and T-bet expressions in T and B cells. According to the immunological pathway knowledge and the mutually verified associations, the following conclusions are made. Expressions of TLR9 and T-bet were increased in patients with SLE. TLR9 may have a role to play in protecting against lupus. And the increase of the co-expression of TLR9 and T-bet may be of benefit to the protective antibodies' production and pathogenic antibodies' decline, and could be regarded as a good sign for lupus demission and/or treatment.