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The results of studies on association between FCGR2A-R/H131 polymorphism and susceptibility to systemic lupus erythematosus (SLE) in the Asian population are controversial. To derive a more precise estimation on the genetic risk of FCGR2A-R/H131 variant for SLE in Asians, a meta-analysis was performed for genotypes R/R + R/H (dominant effect), R/R (recessive effect), and R allele in fixed/random effects models. Twenty studies involving 4,832 SLE patients and 6,190 controls were included. The meta-analysis showed that FCGR2A-R/H131 variant was associated with development of SLE in overall Asians both at allele or genotype level (R vs H, OR 1.201, 95 % CI 1.098-1.315; RR + RH vs HH, OR 1.369, 95 % CI 1.115-1.682; RR vs RH + HH, OR 1.305, 95 % CI 1.029-1.654). After stratification by ethnic, a significant association of R allele with susceptibility to SLE was observed in the Chinese population (R vs H, OR 1.104, 95 % CI 1.030-1.183). Evidence from subgroup analyses in non-Chinese populations (all Asians excluding Chinese population) also showed a significant association (R vs H, OR 1.354, 95 % CI 1.207-1.519; RR + RH vs HH, OR 1.705, 95 % CI 1.234-2.355). In addition, FCGR2A-R131 allele was associated with a 1.186-fold (95 % CI 1.043-1.349) greater risk for the occurrence of nephritis in the Asians population with SLE. After stratification by ethnic, this significant association was only consistently identified in non-Chinese populations (R vs H, OR 1.220, 95 % CI 1.002-1.486). In summary, FCGR2A-R/H131 polymorphism is associated with SLE and lupus nephritis in Asians.

A transmission method , combining both the bit error diversity and joint network-channel coding, was proposed for multiple-user multiple-hop multiple-relay networks. In the poposed method, an interleaver was designed for the bit error diversity and a novel protocol was devised for random linear network coding. The proposed method as well as other two methods—Method I without channel code and protection and Method II only with protection, was analyzed by deriving performance expressions in terms of packet error rate (PER) and throughput. Moreover, simulations further prove the superiority of the proposed method. Numerical results show that the proposed method gains an improvement in PER compared with Method I & II and keeps highest throughput within certain range of SNR.

Systemic lupus erythematosus (SLE) is a severe complex rheumatic disease, but good estimate of its prevalence and risk factors is lacking in China. The aim of the study was to explore the prevalence of SLE and risk factors in rural areas of Anhui Province of China. Eleven counties were randomly selected in Anhui Province, and then, 15% of the villages in selected counties were randomly sampled as study sites. Patients with SLE were identified through two phases. Based on the cases identified, a population-based case-control study was designed to examine risk factors associated with SLE. A total of 1,253,832 individuals and identified 471 SLE cases were surveyed. Crude and age-standardized prevalence were estimated at 37.56 and 36.03 per 100,000 persons, respectively. Gender difference in the prevalence of SLE was significant (P = 4.62 × 10(-76)), and the age-standardized prevalence was 6.17 for males and 67.78 for females per 100,000 persons. The distribution of SLE prevalence was significant by age group (P = 1.78 × 10(-53)), and the peak prevalence was observed at 40-50 years. Multiple environmental factors were associated with SLE, including birth conditions, sweet food, cooking oil, taste, fruit consumption, sunlight exposure, quality of sleep, physical activities, drinking water, residence, negative life events, hepatitis B vaccine, age of menarche, and age at birth of first child (P0.05). Our large population-based epidemiological survey estimated the prevalence of SLE at 37.56 per 100,000 persons. Multiple environmental factors were associated with the development of SLE.

Recently, evidence is emerging that inappropriate regulation of type 17 T helper cells (Th17) plays a fundamental role in the development of many autoimmune diseases including systemic lupus erythematosus (SLE). However, the role of Th17-related cytokines in SLE remains elusive. To further investigate the role and imbalance of Th17-related cytokines in the pathogenesis of SLE. A Quantitative RT-PCR Array (Human Th17 for Autoimmunity & Inflammation PCR Array) analyses were performed to study Th17-related genes expression in peripheral white blood cells of 25 new-onset patients with SLE and 15 healthy subjects. When gene expression for SLE patients was compared to the mean of normal controls, among the 84 target genes related to Th17 pathway, 7 (CXCL1, ICAM1, IL10, IL5, IL8, ISG20, JAK2,) were upregulated and 6 (CD28, CD40LG, S1PR1, IL17RE, IL23R, RORC) downregulated. However, comparisons of mRNA expression of Th17 related cytokines between lupus nephritis (LN) patients and SLE patients without nephritis (SLE non LN) showed no significant difference. In conclusion, SLE patients and normal controls showed different expression of a few genes in Th17 pathway, indicating that the pathway may be involved in the pathogenesis of SLE.

The aim of this study was to examine the association of single-nucleotide polymorphisms (SNPs) in IL-21 gene with susceptibility to systemic lupus erythematosus (SLE) in a Chinese population. A total of 605 independent SLE patients and 666 unrelated healthy controls were recruited for the case-control association study. Two SNPs (rs2221903 and rs907715) within the IL-21 gene intronic region were genotyped by TaqMan SNP allelic discrimination methods. The allele T frequency of SNP rs2221903 in patients and healthy controls was 89.4 % and 86.8 %, respectively [T versus C, odds ratio (OR) = 1.287, 95 % confidence interval (CI) = 1.010-1.640]. No significant differences in genotype frequencies were shown between SLE patients and healthy controls (P value = 0.705, 0.406, respectively). However, the effect of recessive model (TT versus CC + CT, OR = 1.368, 95 % CI = 1.050-1.781) was observed. Distributions of allele and genotype frequencies of the SNP rs907715 showed no significant differences between SLE patients and controls. Analysis of the haplotypes revealed that CC haplotype was significantly associated with SLE (OR = 0.734, 95 % CI = 0.573-0.941). In conclusion, our findings suggest that a SNP (rs2221903) and CC haplotype (rs2221903 and rs907715) of the IL-21 gene is associated with SLE in the Chinese population. However, further studies are needed to determine the functional consequences of this polymorphism with SLE susceptibility.

The aim of this study was to investigate the association of receptor interacting protein 2 (RIP2) single-nucleotide polymorphisms (SNPs) with susceptibility to systemic lupus erythematosus (SLE) in a Chinese population. A case-control study was performed on the SNPs rs16900617 and rs16900627 in 590 Chinese SLE patients and 660 healthy controls. These SNPs were typed by TaqMan allele discrimination assays. We found a significant association of rs16900617 G allele [odds ratio (OR) = 0.54, 95% confidence interval (CI) 0.41-0.72] and rs16900627 G allele (OR = 1.28, 95% CI 1.04-1.58) with SLE. Significant differences in genotype frequency distribution were also found in SLE and control individuals (rs16900617: AG versus AA, OR = 0.59, 95% CI 0.44-0.81; GG versus AA, OR = 0.08, 95% CI 0.01-0.65; AG + GG versus AA, OR = 0.55, 95% CI 0.41-0.75; rs16900627: AG versus AA, OR = 1.51, 95% CI 1.17-1.93; AG + GG versus AA, OR = 1.43, 95% CI 1.13-1.82). Analysis of the haplotypes revealed that two haplotypes of AG and GA were also significantly associated with SLE (OR = 1.37, 95% CI 1.11-1.70; OR = 0.60, 95% CI 0.45-0.79). Our findings suggest that the RIP2 gene polymorphisms may be associated with susceptibility to SLE in the Chinese population.

Cytokine-mediated immunity plays a crucial role in the pathogenesis of various autoimmune diseases including systemic lupus erythematosus (SLE). The recent identification of the dimeric interleukin (IL)-12-related cytokine IL-23 now contributes to our understanding of the fine-tuning of cellular immunity. The critical implication of IL-12 p40 in autoimmune inflammation has long been misinterpreted and until recently have studies revealed that it is IL-23, not IL-12, is the crucial factor in this immune dysregulation. Therefore, targeting of IL-23 or the IL-23 receptor is a potential therapeutic approach for autoimmune diseases including SLE. In this opinion article, we will discuss the biological features of IL-23 and summarize recent advances on the role of IL-23 in the pathogenesis and treatment of SLE.

The aim of this study was to investigate the serum RANTES (regulated on activation, normal T-cell expressed and secreted) level in patients with systemic lupus erythematosus (SLE), and the associations with disease activity and clinical laboratory indexes. Twenty-seven SLE patients and 27 normal controls were enrolled in this study. Serum RANTES was measured by enzyme-linked immunosorbent assay (ELISA). The clinical and laboratory parameters of the patients were also recorded. Results showed that serum RANTES level was significantly elevated in SLE patients when compared with normal controls. Serum RANTES level was correlated with C3, ANA, anti-dsDNA antibodies, anti-Sm antibodies, and anti-SSB antibodies. Nevertheless, no association of serum RANTES level with SLEDAI was found. Taken together, serum RANTES level was significantly higher in SLE patients, suggesting that RANTES might be involved in the pathogenesis of SLE.

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.

The objective was to assess AIDS awareness and condom use in a rural northern Anhui area with a high HIV prevalence. One hundred two AIDS patients underwent a structured interview using a standard questionnaire. There were 51 female and 51 male patients, whose mean age was 46.27 ± 7.27 years and who had good knowledge of AIDS-related issues. More sexually active patients than those nonactive ones knew it more properly that AIDS was a blood-borne disease (100% vs 94.4%; P = 0.03). Significantly more female patients than male (62.7% vs 47.1%; P = 0.047) knew AIDS is incurable. Self-perceived risk was low, and only 84 respondents regarded the condom use as a common problem in their area. Two independent factors associated with a higher rate of condom use were the AIDS patients’ income level and their knowledge about condom use. There was statistically significance between the patients who regularly obtained free condoms and those who did not. The patients who bought condoms on their own initiative had a higher chance of using condoms than those who did not. In conclusion, despite a high level of awareness of HIV/AIDS issues, self-perceived risk was low, condom use was infrequent, and especially men continued to have multiple sexual partners.

Recently, many studies have shown that Single immunoglobulin interleukin-1 receptor related protein (SIGIRR), a member of the IL-1R family acting as a negative regulator of TLR/IL-1R signaling, affects autoimmune responses in animal model of systemic lupus erythematosus (SLE). However, the role of SIGIRR in the pathogenesis of human SLE has not been widely explored. In this study, we analyzed the frequency of SIGIRR-positive CD4+ T cells in peripheral blood mononuclear cells (PBMCs) of SLE patients and its correlation with disease activity as well as the clinical data. Circulating SIGIRR-positive CD4+ T cells were quantified in 51 SLE patients and 38 healthy controls by using flow cytometer. Results showed that the percentages of SIGIRR-positive CD4+ T cells were decreased in the PBMCs of SLE patients compared with healthy controls (Z = −5.49, P

The aim to this study was to investigate the association between the single-nucleotide polymorphisms (SNPs) of interleukin (IL)-23 receptor gene and systemic lupus erythematosus (SLE) in a Chinese population. A case–control study was performed to investigate the associations of SNPs in IL-23R gene (rs10889677 and rs1884444) with susceptibility to SLE in 521 Chinese SLE patients and 527 normal controls. The chi-square test and unconditional Logistic regression were used to analysis by SPSS 10.1 software. No significant differences were detected for the distribution of allele and genotype frequencies of these two SNPs between patients and controls as well as SLE patients with nephritis (LN) and those without nephritis. The findings suggest that the polymorphisms of IL-23R gene might not contribute to the susceptibility of SLE in the Chinese population.

The P2X7 receptor is a ligand-gated cationic channel receptor that is actived by ATP and normally expressed by a variety of immune system cells, including macrophages and lymphocytes. Because it leads to release of IL-1β and cell death by apoptosis or necrosis, it is a potential therapeutic target for a variety of autoimmune inflammatory diseases, such as systemic lupus erythematosus (SLE). The P2X7R gene is highly polymorphic, and many single-nucleotide polymorphisms (SNPs) have been detected. A case-control study was performed to investigate the associations of SNPs in the P2X7R gene (rs1718119, rs2230911 and rs3751143) with susceptibility to SLE in 535 Chinese SLE patients and 532 controls. Results showed that rs1718119 was associated with SLE; in particular carriers of the A allele and AA/AG/(AG+AA) genotypes were at lower risk of the disease [A versus G, P < 0.001, odds ratio (OR) = 0.543, 95% CI: 0.424-0.697; AG versus GG, P = 0.018, OR = 0.659, 95% CI: 0.466-0.931; AA versus GG, P = 0.011, OR = 0.176, 95% CI: 0.046-0.668; AG+AA versus GG, P = 0.004, OR = 0.607, 95% CI: 0.433-0.850], but no significant differences in rs2230911 and rs3751143 were observed between SLE patients and controls. Stratification of cases for the presence of nephritis showed that rs2230911 G allele and CG/(CG+GG) genotypes were at a lower risk of SLE with nephritis (LN) (G versus C, P = 0.011, OR = 0.640, 95% CI: 0.454-0.903; CG versus CC, P = 0.035, OR = 0.645, 95% CI: 0.429-0.970; GG versus CC, P = 0.101, OR = 0.349, 95% CI: 0.099-1.228; CG+GG versus CC, P = 0.015 OR = 0.612, 95% CI: 0.411-0.910), but rs1718119 and rs3751143 were not associated with LN. Analysis of the haplotypes revealed one haplotype (ACA) that appeared to be a significantly 'protective' haplotype (P = 0.009, OR = 0.708, 95% CI: 0.546-0.918) with SLE. The findings suggest that the P2X7R gene might contribute to SLE susceptibility in the Chinese population.

Cytotoxic T lymphocyte associated antigen-4 (CTLA-4) -1722T/C polymorphism has been identified as a susceptibile gene for systemic lupus erythematosus (SLE), but studies are inconsistent. To better assess the association between CTLA-4 -1722T/C polymorphism and SLE, a meta-analysis was performed, including 10 studies, total of 1 387 patients and 1 617 controls. Overall, the CTLA-4 -1722T/C polymorphism was significantly associated with SLE susceptibility (T VS C: OR = 1.17, 95% CI = 0.86-1.60, P = 0.304; T/T VS C/C: OR = 1.92, 95% CI = 1.09-3.39, P = 0.024; T/C VS C/C: OR = 1.50, 95% CI = 0.91-2.49, P = 0.114; T/T VS T/C: OR = 1.29, 95% CI = 0.95-1.75, P = 0.107). When stratified by ethnicity, the CTLA-4 -1722T/C polymorphism was associated with SLE only in Asians (T VS C: OR = 1.47, 95% CI = 1.10-1.96, P = 0.010; T/T VS C/C: OR = 2.09, 95% CI = 1.13-3.85, P = 0.018; T/C VS C/C: OR = 1.53, 95% CI = 0.87-2.69, P = 0.141; T/T VS T/C: OR = 1.42, 95% CI = 0.97-2.09, P = 0.070). In summary, the CTLA-4 -1722T/C polymorphism confers to SLE risk, especially in Asians.

Interleukin 33 (IL-33) is a newly described member of the IL-1 superfamily of cytokines. Through activation of the ST2 receptor, which is widely expressed particularly by helper T 2 cells and mast cells, IL-33 is involved in T-cell–mediated immune responses. Many previous studies have demonstrated that IL-33 may have a pleiotropic function in different diseases, and it could represent a novel target for the treatment of a range of diseases. Recent works have explored the role of IL-33 in chronic autoimmune diseases, such as systemic sclerosis, inflammatory bowel disease, rheumatoid arthritis, and systemic lupus erythematosus. These results indicate that IL-33 may contribute to the pathogenesis of chronic autoimmune diseases. Hence, in this review, we discuss the biological features of IL-33 and summarize recent advances on the role of IL-33 in the pathogenesis and treatment of autoimmune diseases.

This study aimed at understanding the HIV prevalence, distribution of HIV risk factors and whether the HIV has spread from high-risk groups to the general population in the Yanyuan and Muli counties, Liangshan Prefecture, Sichuan Province, China. A multistage probability method was used to select a representative sample of villages in each county, with stratification by risk employed in the sampling for the Yanyuan county. A real-name registration and confidential method were adopted to collect the information of the participants. Blood specimens were tested for HIV, syphilis, and hepatitis C virus. A total of 4,950 subjects participated in the study. Of the participants aged ≥ 15 years, 0.12% self-reported being drug users and 40% were injection drug users; 0.46% had multiple sex partners and the condom use rate was only 26.3% during the last sexual intercourse. HIV, syphilis, and HCV prevalence of Yanyuan county were 0.06% (95% CI: 0-0.142), 0.06% (95% CI: 0-0.142), and 0.15% (95% CI: 0.020-0.280), respectively. HCV prevalence of Muli county was 0.06% (95% CI: 0-0.191), and none was found to be HIV or syphilis positive. Therefore, the rate of HIV infection in Yanyuan and Muli counties is at a low level currently. The Yanyuan county HIV infection rate is similar to the average rate in all of China, and the Muli county rate is below China's average. The HIV epidemic has not spread from high-risk groups to the general population in these two counties.

T helper 17 (TH17) cells are beginning to be implicated in the pathogenesis of systemic lupus erythematosus (SLE). Recent studies have shown that interleukin 27 (IL-27) controls the development of TH17. However, whether IL-27 plays a role in the development of SLE is still unclear. In the present work, we investigated the serum IL-27 level in SLE and its relations to disease activity. Fifty-six patients with SLE and 30 healthy volunteers were recruited. Serum IL-27 levels were detected by enzyme-linked immunosorbent assay. The clinical and laboratory parameters were collected from medical records or by questionnaire. The serum IL-27 level in SLE patients was significantly lower than that in healthy controls ( P < 0.001). Compared with SLE patients without nephritis, patients with nephritis had a significantly decreased serum IL-27 level ( P < 0.05). However, there was no significant difference between less active and more active SLE ( P > 0.05). Correlation analysis between serum IL-27 levels and SLE disease activity index showed no association ( P > 0.05). In summary, a decrease in serum IL-27 level in patients with SLE suggested that this cytokine might be implicated in the pathomechanism of this disease.

Dear Editor, Recently, Kapsimali et al. reviewed the factors involved in the pathogenesis of Behcet's disease (BD) with emphasis on the role of immunological aberrations. The authors concluded that Th1 immune response polarization was a main characteristic when focusing on the influence of cytokines in the etiopathogenesis of BD and suggested that IL-12 may play a central role in the disease immune mechanisms [1]. Indeed genetic factors’ involvement has been investigated. The findings showed that Th1 cytokines (including IL-12 and IFN-γ) polymorphisms were associated with susceptibility to BD [2]. However, as we know, IL-12 shares a p40 subunit with IL-23, which has additional inflammatory effects apart of IL-12. In fact, update data have suggested that IL-23/IL-17 axis may be crucial to BD development. A previous study has shown higher IL-23 in sera of BD patients with uveitis and found that there was a meaningful correlation between IL-23 content and disease activity [3]. Moreover, Lew et al. reported an increased expression of IL23 p19 mRNA in erythema nodosum-like lesions of BD patients [4]. Furthermore, Chi et al. showed that the expression of IL-23p19 mRNA, IL-23, IL-17, and IFN-γ was markedly elevated in BD patients with active uveitis. Meanwhile, the frequencies of IL-17-producing and IFN-γproducing T cells from PBMCs were significantly upregulated in BD patients with active uveitis. These findings hinted that the IL-23/IL-17 pathway together with IFN-γ was associated with the active intraocular inflammation in BD [5]. In addition, authors also identified IL-23R and IL-17F gene polymorphisms which were associated with susceptibility to BD [6, 7]. Collectively, not only IL-12/IFN-γ axis but also IL-23/ IL-17 pathway may make a contribution for immunological aberrations of BD. Therefore, further studies are required to comprehensively explore the role of Th17 immune response in the etiopathogenesis of BD.