Wang-Dong Xu

Anhui Medical University, Luchow, Anhui Sheng, China

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Publications (43)121.66 Total impact

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    ABSTRACT: Objective: The aim of this study was to determine whether caspase recruitment domain-containing protein 8 (CARD8) rs2043211 polymorphism was associated with susceptibility to inflammatory bowel disease (IBD). Methods: Relevant studies were searched using PubMed and Embase up to February 2014. A meta-analysis was conducted on the association between rs2043211 polymorphism and IBD using: (1) allele contrast, (2) the dominant model, (3) the recessive model, and (4) homozygote contrast. The pooled estimated of risk was obtained by random-effects model or fixed-effects model. Publication bias was assessed by Egger's test. Results: Eight relevant articles with a total of 10 534 IBD patients [6785 Crohn's disease (CD), 3713 ulcerative colitis (UC) and 36 indeterminate colitis (IC)] and 6755 healthy controls were included in the meta-analysis, which consisted of 12 studies, 12 for CD, 10 for UC, 2 for IC. There was no significant association between rs2043211 polymorphism and IBD, CD, and IC in overall population. However, stratified meta-analysis by ethnicity showed significant association between rs2043211 polymorphism and CD in the European population under the dominant model [odds ratio (OR) = 1.210, 95% confidence interval (CI) = 1.013-1.445, p = 0.036] and homozygote contrast (OR = 1.212, 95% CI = 1.005-1.461, p = 0.044). Conclusions: Our meta-analysis results indicated significant association between rs2043211 polymorphism and the susceptibility to CD under the dominant model and homozygote contrast in the European population.
    Immunological investigations 01/2015; DOI:10.3109/08820139.2014.988721 · 1.90 Impact Factor
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    ABSTRACT: Abstract T-cell immunoglobulin domain and mucin domain-4 (Tim-4) was first recognized as a costimulatory molecule regulating T-cell activation. Dysregulation of Tim-4 has been found in some autoimmune conditions, particularly in the immune cells. Recently, Tim-4 was found to be critical for regulating T cells, with the ability of inhibiting naïve CD4(+) T cells and Th17 cells, increasing Th2 cell development. Tim-4 can also enhance T cell expansion via linker for activation of T cells, extracellular signal-regulated kinase (ERK) and Protein kinase B (PKB, also known as Akt) signaling pathways. Moreover, the Tim-4 signaling pathway may affect multiple molecular processes in autoimmune diseases. A number of previous studies have demonstrated that Tim-4 influences chronic autoimmune diseases, such as rheumatoid arthritis (RA) and systemic lupus erythematosus. In addition, an association between Tim-4 polymorphisms and susceptibility to several autoimmune diseases have been identified, such as RA. Taken together, recent works have indicated that Tim-4 may represent a novel target for the treatment of autoimmune diseases. In this article, we will discuss the Tim-4 function and the therapeutic potential of modulating the Tim-4 in autoimmune diseases.
    Autoimmunity 11/2014; DOI:10.3109/08916934.2014.983266 · 2.75 Impact Factor
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    ABSTRACT: Previous studies investigating the association between 5,10-methylenetetrahydrofolate reductase (MTHFR) gene polymorphisms and colon cancer risk have generated conflicting results. The aim of our meta-analysis was to clarify the precise association. A systematic literature search was conducted to identify all relevant studies. Pooled odds ratio (ORs) with 95% confidence interval (CI) were used to estimate the strength of the association. In this meta-analysis, a total of 13 articles, involving 5,386 cases and 8,017 controls met the inclusion criteria. Overall, a significant association was found between colon cancer risk and the MTHFR C667 polymorphism (TT vs CC+CT: OR=0.79; 95%CI=0.65-0.96; p=0.017). Stratification by ethnicity revealed that MTHFRC667 was associated with colon cancer risk in the non-Asian group (TT vs CC+CT:OR=0.77, 95%CI=0.68-0.89, p=0.000; TT vs CC: OR=0.84, 95%CI=0.73-0.97, p=0.016). Stratification by source of control indicated that MTHFR C667 also correlated with colon cancer risk in the population-based subgroup (TT vs CC: OR=0.85, 95%CI=0.74-0.97, p=0.017; TT vs CC+CT: OR=0.78, 95%CI=0.68-0.89, p=0.000) and hospital-based subgroup (TT vs CC+CT: OR=0.65, 95%CI=0.49-0.86, p=0.003). However, risk was significantly increased for MTHFR A1298C polymorphisms and colon cancer risk in hospital-based studies (C vs A: OR=1.52, 95%CI=1.26-1.83, p=0.000; CC+AC vs AA: OR=1.93, 95%CI=1.47-2.49, p=0.000) but reduced in population-based studies (CC vs AA: OR=0.83, 95%CI=0.70-0.99, p=0.042). In conclusion, the results of our meta-analysis suggest that the MTHFR C667 polymorphism is associated with reduced colon cancer risk, especially for non-Asian populations.
    Asian Pacific journal of cancer prevention: APJCP 10/2014; 15(19):8245-50. DOI:10.7314/APJCP.2014.15.19.8245 · 1.50 Impact Factor
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    ABSTRACT: The aim of this study was to investigate the mRNA expression levels of suppressor of cytokine signaling 1 (SOCS1) in patients with systemic lupus erythematosus (SLE) compared with healthy controls. The associations of systemic lupus erythematosus disease activity index scores and clinical features of SLE with the expression levels of SOCS1 mRNA were also evaluated. Real-time quantitative reverse transcription-polymerase chain reaction was applied to detect the mRNA expression levels of SOCS1 in peripheral blood mononuclear cells from 34 patients with SLE and 34 healthy controls. The mRNA expression level of SOCS1 was significantly decreased in SLE patients in comparison with healthy controls (Z = -4.207, P < 0.001). Lower SOCS1 mRNA expression was detected in active SLE patients when compared with inactive ones (Z = -2.428, P = 0.015). There was no significant difference found for the SOCS1 mRNA levels between SLE patients with nephritis and those without (Z = -0.642, P = 0.521). The presence of photosensitivity, proteinuria, positive antinuclear antibody, and C4 decline were associated with SOCS1 mRNA levels in SLE patients (all P < 0.05). Furthermore, the SOCS1 mRNA expression was negatively correlated with disease activity (r s = -0.372, P = 0.030). Our results suggest that the dysregulation of SOCS1 might be associated with the pathogenesis of SLE.
    Clinical and Experimental Medicine 10/2014; DOI:10.1007/s10238-014-0309-2 · 2.82 Impact Factor
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    ABSTRACT: The aim of this study was to determine the risk factors for avascular necrosis (AVN) in patients with systemic lupus erythematosus (SLE). Four electronic databases (PubMed, EMBASE, Ovid, and Science Direct) were searched for. The search was performed to identify the articles as to SLE with AVN before September 2013. The clinical and laboratory data were extracted, and a meta-analysis was performed to identify the risk factors for AVN in patients with SLE. Publication bias was assessed with funnel plot and Egger's test. A total of 995 papers were found from the four databases; 16 studies were finally included. Pooled analysis showed the following result. The result showed that arthritis (odds ratio (OR) = 2.448, 95 % confidence interval (CI) = 1.617-3.707), cushingoid (OR = 3.890, 95 % CI = 1.591-9.510), gastrointestinal involvement (OR = 2.054, 95 % CI = 1.283-3.290), hypertension (OR = 1.482, 95 % CI = 1.093-2.008), oral ulcers (OR = 1.877, 95 % CI = 1.182-2.979), pleuritis (OR = 2.302, 95 % CI = 1.325-4.001), renal disease (OR = 1.475, 95 % CI = 1.124-1.936), and vasculitis (OR = 2.591, 95 % CI = 1.358-4.944) were relevant with AVN in SLE patients. Cytotoxic drug (OR = 1.834, 95 % CI = 1.065-3.156, P = 0.029), the total cumulative dose (Standard Mean Difference (SMD) = 1.104, 95 % CI = 0.118-2.090, P = 0.028), maximum daily dose (SMD = 0.484, 95 % CI = 0.288-0.678, P < 0.001), and mean daily dose (SMD = 1.305, 95 % CI = 0.061-2.549, P = 0.040) were significantly higher in AVN group. There were no significantly laboratory features that appeared in this pooled analysis. We conclude that arthritic, cushingoid, gastrointestinal involvement, hypertension, oral ulcers, pleuritis, renal disease, vasculitis, cytotoxic drug, and steroid treatment may contribute to AVN in SLE patients.
    Inflammation 05/2014; 37(5). DOI:10.1007/s10753-014-9917-y · 1.92 Impact Factor
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    ABSTRACT: Introduction: Tyrosine kinase 2 (Tyk2) is a Janus kinase family member that is crucial for signaling transduction in response to a wide variety of cytokines, including type I IFNs, IL-6, IL-10, IL-12 and IL-23. An appropriate expression of Tyk2-mediated signaling might be essential for maintaining normal immune responses. Areas covered: This review summarizes that Tyk2 is essential for the differentiation and function of a wide variety of immune cells, including natural killer cells, B cells, as well as T helper cells. In addition, Tyk2-mediated signaling promoted the production of autoimmune-associated components, which is implicated in the pathogenesis of autoimmune diseases, such as rheumatoid arthritis, systemic lupus erythematosus, multiple sclerosis. Aberrant expression of Tyk2 was observed in many autoimmune conditions. Expert opinion: Until recently, no patent filings had claimed selective inhibitors of Tyk2. Both CP-690,500 and CMP6 failed to be used in clinical treatment due to the difficulties of finding suitable selective leads or due to detrimental toxicities. Although the result of Cmpd1 is promising, it remains to be seen how specific the Tyk2 inhibitor is and how they are working. Currently, structure-based drug design (SBDD) technology has provided us with a quite useful window for SBDD of Tyk2 inhibitors.
    Expert Opinion on Therapeutic Targets 03/2014; DOI:10.1517/14728222.2014.892925 · 4.90 Impact Factor
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    ABSTRACT: Stigma is a common problem among people living with HIV/AIDS (PLWHA). However, little is known about HIV/AIDS-related stigma in older PLWHA over the age of 50. This study described the stigma of HIV/AIDS and its factors based on 120 PLWHA aged 50 or older in an area of high HIV prevalence in south rural China. Each participant completed a face-to-face questionnaire that collected information on demographic characteristics, AIDS-related events and experience of HIV/AIDS-related stigma. Finally, only 18.1% reported experiencing external stigma compared with 64.3% feeling internal stigma. Regression analysis indicated that social support and health status were the two variables that were significantly predictive of both external and internal stigma. Whatever, the more support were received from family members by PLWHA, the less external stigma was perceived. Negative marital situation was also related to external stigma. Reducing HIV/AIDS stigma requires a supportive environment, positive attitude and correct knowledge of AIDS. Health workers and policy makers should take practical approaches to reduce prejudice.
    International Journal of Nursing Practice 03/2014; DOI:10.1111/ijn.12254 · 0.54 Impact Factor
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    ABSTRACT: Abstract Systemic lupus erythematosus (SLE) is complex autoimmune disease which involves various facets of the immune system. Signaling transducers and activators of transcription 1 (STAT1) belongs to the family of STAT transcription factors that mediate various biological responses. Recently, studies in both experimental animal models of lupus and patients with SLE have revealed expression and activation of STAT1 is closely associated with the pathogenesis of SLE. Moreover, increased production of interferons (IFNs) and aberrant activation of IFNs signaling, which is mechanistically linked to increased level of STAT1, are crucial for the development of SLE. Therefore, we will focus on the association of STAT1 and SLE based on recent understandings to render more information about the mechanisms of STAT1 might perform in. Hopefully, the information obtained will lead to a better understanding of the development and pathogenesis of systemic autoimmune diseases, as well as its clinical implications and therapeutic potential.
    Autoimmunity 01/2014; DOI:10.3109/08916934.2013.873415 · 2.75 Impact Factor
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    ABSTRACT: The aim of this study was to determine whether CTLA-4 gene variants were associated with susceptibility to inflammatory bowel disease (IBD). Meta-analysis was conducted on the association between CTLA-4 variants and IBD using: 1) allelic contrast, 2) the recessive model, and 3) the dominant model. A total of 9 relevant studies including 1,739 Crohn's disease (CD) cases, 10 relevant studies containing 1,017 ulcerative colitis (UC) cases and 2,685 healthy controls were involved in this meta-analysis. Overall, CTLA-4 +49A/G, -318C/T and CT60 variants were not associated with IBD susceptibility in all genetic models (P > 0.05). Stratification by ethnicity indicated a significant association between the CTLA-4 +49A/G variant and CD in Caucasian group (GG vs. GA + AA: OR = 0.723, 95% CI = 0.564-0.926, P = 0.010). In Asian group, meta-analysis showed a significant association between the CTLA-4 CT60 variant and UC (AA vs. AG + GG: OR= 0.375, 95% CI = 0.163-0.861, P = 0.021). Based on the published literature, this meta-analysis suggests that the CTLA-4 +49A/G variant may be related to CD susceptibility in Caucasians, and the CTLA-4 CT60 variant may be associated with UC susceptibility in Asians.
    Human immunology 12/2013; 75(3). DOI:10.1016/j.humimm.2013.12.008 · 2.28 Impact Factor
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    ABSTRACT: The aim of this study was to perform a meta-analysis of eligible studies to derive precise estimation of the association of interleukin-1 (IL-1), IL-10 and tumor necrosis factor (TNF)-α polymorphisms with Behcet's disease (BD). Odds ratios (ORs) and 95% confidence intervals (CIs) were used to assess the strength of the association. A total of 4003 cases and 4748 controls in 19 eligible studies were included in the meta-analysis. We examined the relationship between seven single nucleotide polymorphisms (SNPs) in the above-mentioned three cytokine genes and susceptibility to BD. Meta-analysis indicated the association between the cytokine gene polymorphisms in all study subjects in the allelic model (TNF-α -308A/G: OR = 0.73, 95% CI: 0.61-0.88, P = 0.001; IL-10 -819C/T: OR = 0.72, 95% CI: 0.66-0.78, P < 0.001; IL-10 -592C/A: OR = 0.74, 95% CI: 0.64-0.86, P < 0.001); the dominant model (TNF-α -308A/G: OR = 0.77, 95% CI: 0.64-0.92, P = 0.004; IL-10 -1082G/A: OR = 1.64, 95% CI: 1.10-2.44, P = 0.014); the recessive model (TNF-α -308A/G: OR = 0.27, 95% CI: 0.12-0.65, P = 0.003; IL-10 -819C/T: OR = 0.71, 95% CI: 0.57-0.90, P = 0.004). However, no significant evidence for the associations of IL-1α -889C/T, IL-1β -551C/T, IL-1β -3962C/T polymorphisms with BD susceptibility was detected. The present study might suggest that TNF-α -308A/G, IL-10 -1082G/A, -819C/T, -592C/A polymorphisms are associated with BD susceptibility.
    International Journal of Rheumatic Diseases 11/2013; 16(6). DOI:10.1111/1756-185X.12221 · 1.77 Impact Factor
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    ABSTRACT: Emerging evidences were accumulated to support the view that aberrant interleukin-7 (IL-7) signaling might be associated with autoimmunity. Former studies demonstrated the single nucleotide polymorphism (SNP) rs6897932 C/T in the IL-7 receptor (IL-7R) gene was associated with susceptibility to autoimmune diseases, including multiple sclerosis and type I diabetes. Given these, this study was conducted to investigate whether an association existed between SNP rs6897932 and the susceptibility to systemic lupus erythematosus (SLE), a severe systemic autoimmune disease. In this context, 816 SLE patients and 816 controls from a Chinese population were recruited for this study, and the results showed that the major allele C of rs6897932 showed a higher frequency in SLE patients compared with controls (P = 0.039, C versus T); significant difference was also detected under a recessive model with regard to the distribution of genotype frequencies between SLE patients and controls (P = 0.041, CC versus CT + TT), which was not consistent with the results under a dominant model (P = 0.349, CC + CT versus TT). Moreover, association studies were also performed contraposing the relationship between the SNP rs6897932 C/T and lupus nephritis as well as 10 clinical features of SLE; however, no significant association signal was found regarding the distribution of allele and genotype frequencies between SLE patients positive and negative for the presence of 11 sub-phenotypes. In conclusion, the major allele C of SNP rs6897932 may be associated with increased SLE risk in Chinese populations, and further studies are still encouraged to shed light on the true associations between SLE and its susceptibility genes with respect to IL-7R gene.
    Inflammation 11/2013; DOI:10.1007/s10753-013-9777-x · 1.92 Impact Factor
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    ABSTRACT: Hypoxia-inducible factor 1 (HIF-1) introduced the immune imbalance between Th17 and Treg cells, which may play an important role in the pathogenesis of systemic lupus erythematosus (SLE). The aim of the present study was to determine whether the HIF1A gene influences the susceptibility to SLE. A study on this relationship has not been conducted to date. A total of 3,793 subjects (1,497 SLE patients and 2,296 controls) were included in this study. The genotyping of five single-nucleotide polymorphisms (SNPs) (rs11549465, rs12434438, rs1957757, rs1951795, rs7143164) was determined by Sequenom MassARRAY technology. The statistical analysis was conducted using chi-square test. Odds ratio (OR) with 95 % confidence interval (CI) was calculated using unconditional logistic regression with adjustment of age and sex. The allele frequencies were not associated with the disease. No significant differences in genotype frequencies existed between the patients with SLE and the controls in all five SNPs. It is worth mentioning that the allele T at rs11549465, located at the exon sequence, revealed a trend but no significant difference towards the more frequent allele T in SLE than in controls (C versus T: OR = 1.206, 95 % CI = 0.972-1.495, p = 0.088). The genotype effects of recessive, dominant, and codominant models were observed; however, no significant evidence for association was detected. Our findings suggest that the gene polymorphisms of HIF1A might not contribute to SLE susceptibility in the Chinese population. However, further studies are needed on an independent cohort from different genetic backgrounds to confirm HIF1A as an SLE genetic factor.
    Immunogenetics 11/2013; DOI:10.1007/s00251-013-0743-4 · 2.49 Impact Factor
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    ABSTRACT: Studies investigating the association between the tumor necrosis factor (TNF) gene polymorphisms and Behcet's disease (BD) report conflicting results. The aim of this meta-analysis was to assess the association between TNF gene polymorphisms and BD. A systematic literature search was conducted to identify all relevant studies. Pooled odds ratios (ORs) with 95% confidence intervals (CIs) were used to estimate the strength of the association. A total of 16 articles, involving 1,708 patients with BD and 1,910 healthy controls, were included in the meta-analysis. Overall, a significant association was found between BD and the TNF -308A/G polymorphism (OR=0.730, 95% CI=0.608-0.877, p=0.001). Meta-analysis of TNF -238A/G showed significant association with BD (OR=1.512, 95% CI=1.155-1.979, p=0.003). The TNF -1031C allele showed significant association with BD (OR=1.549, 95% CI=1.190-2.015, p=0.001). Similarly, the meta-analysis showed a significant association of the TNF -857T/C polymorphism with BD (OR=0.758, 95% CI=0.593-0.968, p=0.027). Stratification by ethnicity revealed that the -308A/G and -857T/C polymorphisms were associated with BD in the Asian group, while the -238A/G and -1031C/T polymorphisms were associated with BD in the Caucasian population. The results of our meta-analysis suggest that TNF (-308A/G, -238A/G, -1031C/T, and -857T/C) polymorphisms are associated with susceptibility to BD.
    Molecular vision 09/2013; 19:1913-24. · 2.25 Impact Factor
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    ABSTRACT: Le but de cette étude était de déterminer si le polymorphisme nucléotidique de l’interleukine (IL)-6-174 confère une susceptibilité à la polyarthrite rhumatoïde (PR) et au diabète de type 1 (DT1) dans des populations multiethniques.MéthodesUne méta-analyse fut conduite sur l’association entre le polymorphisme IL-6-174 et la susceptibilité PR/DT1 en utilisant des modèles à effets fixes et aléatoires.RésultatsTreize études furent incluses dans la méta-analyse : PR sept études, incluant six populations européennes et une asiatique ; DT1 : six études incluant cinq populations européennes et une sud-américaine. Il n’y avait pas d’association significative dans les comparaisons, à la fois entre les allèles et les génotypes, entre le polymorphisme IL-6-174 et les PR/DT1 chez les sujets de toutes les études. De plus, la méta-analyse stratifiée par ethnies indique l’absence d’association entre le gène et les PR/DT1.Conclusion Cette méta-analyse suggère que le polymorphisme génétique IL-6-174 pourrait ne pas conférer une prédisposition à la PR et au DT1.
    Revue du Rhumatisme 07/2013; 80(4):373-377. DOI:10.1016/j.rhum.2013.01.008
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    ABSTRACT: Rheumatoid arthritis (RA) is characterized by chronic inflammatory disease, including synovial proliferation and excessive pro-inflammatory cytokines production, leading to cartilage and bone destruction. Cytokine-mediated immunity plays an important role in the pathogenesis of various autoimmune diseases such as RA. Recently, the IL-1 family member IL-33, was recognized to perform as an inflammatory cytokine, exerted profound effects in human RA and experimental inflammatory arthritis. Furthermore, inhibition of IL-33 signaling proposed a potential therapeutic approach. In this review, we summarize recent advances on the pathological roles of IL-33 in RA and discuss the therapeutic significance of these new findings.
    Human immunology 06/2013; DOI:10.1016/j.humimm.2013.06.029 · 2.28 Impact Factor
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    ABSTRACT: Abstract Autoimmune diseases arise from an inappropriate immune response against self components, including macromolecules, cells, tissues, organs etc. They are often triggered or accompanied by inflammation, during which the levels of granulocyte macrophage colony-stimulating factor (GM-CSF) are elevated. GM-CSF is an inflammatory cytokine that has profound impact on the differentiation of immune system cells of myeloid lineage, especially dendritic cells (DCs) that play critical roles in immune initiation and tolerance, and is involved in the pathogenesis of autoimmune diseases. Although GM-CSF was discovered decades ago, recent studies with some new findings have shed an interesting light on the old hematopoietic growth factor. In the inflammatory autoimmune diseases, GM-CSF redirects the normal developmental pathway of DCs, conditions their antigen presentation capacities and endows them with unique cytokine signatures to affect autoimmune responses. Here we review the latest advances in the field, with the aim of demonstrating the effects of GM-CSF on DCs and their influences on autoimmune diseases. The summarized knowledge will help to design DC-based strategies for the treatment of autoimmune diseases.
    Autoimmunity 06/2013; DOI:10.3109/08916934.2013.803533 · 2.75 Impact Factor
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    ABSTRACT: 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.
    Clinical and Experimental Medicine 05/2013; 14(3). DOI:10.1007/s10238-013-0240-y · 2.82 Impact Factor
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    ABSTRACT: Leptin, the product of ob gene, is a 16-kDa nonglycosylated peptide hormone produced by adipocytes that regulates appetite and energy expenditure at the hypothalamic level. As is known to be a satiety factor that can regulate body weight by inhibiting food intake and stimulating energy expenditure, leptin is a pleiotropic hormone whose multiple effects include regulation of endocrine function, reproduction and immunity. Since leptin has been considered to be a pro-inflammatory cytokine, investigations of leptin in the pathogenesis of autoimmune diseases have been detected, such as systemic lupus erythematosus, rheumatoid arthritis and osteoarthritis. Recently, the role of leptin in the modulation of immune response and inflammation has been discussed in the autoimmune diseases increasingly but less in systemic lupus erythematosus (SLE). Therefore, this article will focus on the current understanding of the role of leptin with such similar pathogenic mechanism in SLE in order to provide insights which may assist in the development of leptin-based approaches for the treatment of SLE.
    Rheumatology International 05/2013; 34(4). DOI:10.1007/s00296-013-2774-4 · 1.63 Impact Factor
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    ABSTRACT: OBJECTIVE: The aim of this study was to determine whether the interleukin (IL)-6 -174 single nucleotide polymorphism confers susceptibility to rheumatoid arthritis (RA) and type 1 diabetes (T1D) in multiple ethnic populations. METHODS: A meta-analysis was conducted on the association between the IL-6 -174 polymorphism and RA/T1D susceptibility, using fixed and random effects models. RESULTS: Thirteen studies were included in the meta-analysis: RA: seven studies, including six European and one Asian population; T1D: six studies, including five European and one South American population. There was no significant association both in allele and genotype comparisons between the IL-6 -174 polymorphism and RA/T1D in all study subjects. Moreover, meta-analysis stratified by ethnicity indicated no significant association between the gene and RA/T1D. CONCLUSIONS: This meta-analysis suggests that the IL-6 -174 polymorphism might not confer susceptibility to RA/T1D.
    Joint, bone, spine: revue du rhumatisme 04/2013; 80(5). DOI:10.1016/j.jbspin.2012.11.005 · 3.22 Impact Factor
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    ABSTRACT: Introduction: Small, non-coding, microRNAs (miRNAs) have emerged as key mediators of post-transcriptional gene silencing in both pathogenic and pathological aspects of disorders. Recently, miR-21 was identified to regulate a variety of immune cells. Functional analysis indicated that miR-21 played a crucial role in a plethora of biological functions and diseases including development, cancer and inflammation, especially correlated with the pathogenesis of autoimmune diseases. Areas covered: This review provides a comprehensive view on the association of miR-21 and autoimmune disorders, such as type 1 diabetes, multiple sclerosis, systemic lupus erythematosus, systemic sclerosis and psoriasis. Especially the mechanisms of miR-21 perform in these diseases, and the mechanisms that regulate miR-21. Expert opinion: Though the exact roles of miR-21 in autoimmune diseases have not been fully elucidated, targeting miR-21 may serve as a promising therapy strategy.
    Expert Opinion on Therapeutic Targets 03/2013; DOI:10.1517/14728222.2013.773311 · 4.90 Impact Factor