Systemic lupus erythematosus (SLE) is characterized by aberrant production of auto-antibodies and a sexual dimorphism both in the phenotypic expression and frequency of the disease between males and females. The striking female predominance was initially attributed primarily to sex hormones. However, recent data challenge this simplistic view and point more towards genetic and epigenetic factors accounting for this difference. More specifically, several SLE-associated single-nucleotide polymorphisms (SNPs) have been found to play an important role in the gender predilection in SLE. Their effect is mediated through their involvement in sex-hormone and immune system signalling and dysregulation of the expression of genes and miRNAs pertinent to the immune system. Additionally, the genetic factors are interchangeably associated with epigenetic modifications such as DNA methylation and histone modification, thus revealing a highly complex network of responsible mechanisms. Of importance, disturbance in the epigenetic process of X chromosome inactivation in females as well as in rare X chromosome abnormalities leads to increased expression of X-linked immune-related genes and miRNAs, which might predispose females to SLE. Microbiota dysbiosis has also been implicated in the sexual dimorphism by the production of oestrogens within the gut and the regulation of oestrogen-responsive immune-related genes. Sexual dimorphism in SLE is an area of active research, and elucidation of its molecular basis may facilitate ongoing efforts towards personalized care.

https://journals.sagepub.com/doi/pdf/10.1177/0961203318815768

Sexual dimorphism in SLE: above and beyond sex hormones.

Objective 
To characterize the significance of correlated autoantibodies in systemic lupus erythematosus (SLE) and its complication lupus nephritis (LN) in a large cohort of patients.


Methods 
Clinical data were statistically analyzed in 1699 SLE patients with or without nephritis who were diagnosed and treated during 2002–2013 in the northeast region of China. Reactivity to a list of 16 autoantibodies was detected by the serum test Euroline ANA profile (IgG). Serum titers of the anti-nucleosome autoantibodies were measured by ELISA assays. Kidney biopsies were examined by pathologists. Immune complex deposition was identified by immunohistochemistry stain.


Results 
Simultaneous positivity of anti-dsDNA, -nucleosome and -histone antibodies (3-pos) was prevalent in SLE patients with LN compared to Non-renal SLE patients (41% vs 11%, p< 0.001). Significant correlations were found between any two of the above three anti-nucleosome antibodies in LN patients. In comparison to non-3-pos cohorts, 3-pos patients with LN had significantly higher serum levels of the three antibodies and more active disease; was associated with type IV disease; suffered from more severe renal damages; received more intensive treatment and had worse disease outcome. The serum levels of these three autoantibodies in 3-pos LN patients were significantly decreased when they underwent clinical recovery.


Conclusions 
Simultaneous reactivity to anti-dsDNA, -nucleosome and -histone antibodies by Euroline ANA profile (IgG) may indicate severe nephropathy in patients with SLE.

/pdf/co-positivity-for-anti-dsdna-nucleosome-and-histone-k9tgkel6x6.pdf

Co-Positivity for Anti-dsDNA, -Nucleosome and -Histone Antibodies in Lupus Nephritis Is Indicative of High Serum Levels and Severe Nephropathy

Systemic lupus erythematosus (SLE) is an autoimmune disease involving multiple organ systems with diverse presentation, primarily affecting women of reproductive age. Various genetic and environmental risk factors are involved in the pathogenesis of SLE, and many SLE susceptibility genes have been identified recently; however, gene therapy is not a viable clinical option at this time. Thus, environmental risks factors, particularly regional characteristics that can be controlled, need to be further investigated. Here, we systematically explored these risk factors, including ultraviolet radiation, seasonal distribution, geographical distribution, and climate factors, and also summarized the mechanisms related to these risk factors. Probable mechanisms were explicated in at least four aspects including inflammatory mediators, apoptosis and autophagy in keratinocytes, epigenetic factors, and gene-environment interactions. This information is expected to provide practical insights into these risk factors in order to benefit patients with SLE and facilitate the development of potential therapeutic strategies.

Mechanistic insights into environmental and genetic risk factors for systemic lupus erythematosus.

Long non-coding RNA Xist contribution in systemic lupus erythematosus and rheumatoid arthritis.

Seasonal variations of systemic lupus erythematosus flares in southern France

Systemic lupus erythematosus (SLE) is the prototype of human autoimmune disease in which various inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1, IL-6 and interferon (IFN) play crucial pathogenic roles. The production of these cytokines is responsible for the mitogen-activated protein kinases (MAPKs), which can also generate mitogen-activated protein kinases phosphatases (MKPs). MKP-1, a prototypical member of the MKP family that can influence outcomes of autoimmune diseases and reduce the inflammatory cytokines by dephosphorylation of p38 and JNK MAPK, plays a critical role in the expression of inflammatory mediators at transcriptional and post-transcriptional levels. MicroRNA-101 (miR) is a small non-coding RNA that regulates the MAPK response by targeting MKP-1 mRNA 3'-UTR, and affects the secretion of the downstream inflammatory cytokines. However, the interaction among the above three in the pathogenesis of SLE has not previously been reported. This review discusses the current understanding of the role of the MAPK/MKP/miR-101 axis in regulating immune responses and the pathogenesis of SLE to provide new ideas for clinical treatment of SLE.

MicroRNA-101, mitogen-activated protein kinases and mitogen-activated protein kinases phosphatase-1 in systemic lupus erythematosus.

Summary
Background

IgE plays a important role in systemic lupus erythematosus (SLE). A recent study identified the high-affinity IgE receptor α-chain (FceRIα) gene FCER1A as a susceptibility locus influencing total serum IgE levels.



Aim

To investigate whether the single-nucleotide polymorphism (SNP) rs2298804 (251 A>G) of FCER1A is associated with SLE and its clinical characteristics in a Chinese Han population.



Methods

This case–control study enrolled 948 patients with SLE and 976 healthy controls. Precise phenotyping of patients was accomplished by means of a questionnaire and clinical examination. rs2298804 was genotyped using real-time fluorescence quantitative PCR.



Results

Compared with the healthy controls, patients with SLE had much lower frequencies of the AG genotype (OR = 0.26; 95% CI 0.194–0.374; P << 0.001) and G allele (OR = 0.45; 95% CI 0.36–0.55; P << 0.001). We also found a stronger association of the FCER1A exon SNP, rs2298804 (A/G), in females (OR = 0.42; 95%CI 0.34–0.53; P << 0.001) compared with males (OR = 0.52; 95% CI 0.28–0.97; P < 0.04). G-allele carriers are less likely to develop SLE than A-allele carriers. Although we did not find any significant correlation between the rs2298804 and the incidence of lupus nephritis, rs2298804 seemed to protect against proteinunia, fever and hypocomplementaemia in patients with SLE, but appeared to be a risk factor for photosensitivity and vasculitis.



Conclusions

We found that rs2298804 seemed to have a protective effect against SLE in Chinese patients, especially women. It also protected against proteinunia, fever and hypocomplementaemia, but was a risk factor for photosensitivity and vasculitis.

Sex-specific differences in the relationship between the single-nucleotide polymorphism rs2298804 of FCER1A and the susceptibility to systemic lupus erythematosus in a Chinese Han population.

Tumour suppressor protein 53 (p53) plays a central role in apoptosis, cell proliferation and death. Previously studies found contribution of functional p53 Arg72Pro polymorphism (TP53 rs1042522G/C polymorphism) in the development of systemic lupus erythematosus (SLE) remains controversial. In this study, for the first time, we evaluated its association with SLE in a Chinese Han population. This case–control study enrolled 1470 SLE patients and 2283 healthy controls. The genotyping of TP53 rs1042522 polymorphism was determined by Sequenom Mass ARRAY technology. Statistical analysis was conducted by Chi-square test (χ
 2 test). Odds ratio (OR) with 95% confidence interval (CI) was calculated using unconditional logistic regression with adjusting age and sex. Allele and genotype frequencies of TP53 rs1042522G/C polymorphism showed statistically significant difference between the SLE patients and the normal controls (C vs. G: OR = 0.89, 95% CI 0.89–0.97, p = 0.01; (GC + CC) vs. GG using recessive model: OR = 0.84, 95% CI 0.73–0.96, p = 0.01; GC vs. GG using co-dominant model: OR = 0.86, 95% CI 0.74–0.99, p = 0.04; CC vs. GG using co-dominant model: OR = 0.80, 95% CI 0.66–0.96, p = 0.02; GC vs. GG using co-dominant model: OR = 0.86, 95% CI 0.74–0.99, p = 0.02). In addition, there was weak association between discoid rash and distribution of TP53 rs1042522G/C polymorphism in SLE patients (C vs. G: OR = 1.25, 95% CI 1.00–1.55, p = 0.04; CC vs. GG using co-dominant model: OR = 1.54, 95% CI 1.10–2.36, p = 0.04). Our finding suggests a significant relationship between the TP53 rs1042522G/C polymorphism and SLE. TP53 rs1042522G/C polymorphism would be promising as an indicator of SLE as well as the therapeutic target if its functions and mechanisms could be further investigated.

Association study between the TP53 Rs1042522G/C polymorphism and susceptibility to systemic lupus erythematosus in a Chinese Han population.

Low biomass yield and nutrient removal efficiency are problems challenging the employment of microorganisms for wastewater remediation. Starch processing effluent (SPE) was used as a fermentation substrate to co-culture Chlorella vulgaris and Rhodotorula glutinis for biofuel feedstock production. Co-culture options were compared, and the optimal conditions were identified. The result shows that microalgae and yeast should be inoculated simultaneously at the beginning of SPE-based fermentation to achieve high biomass yield and the optimal inoculation ratio, light intensity, and temperature should be 2:1, 150 μmol/m2/s, and 25 °C, respectively. Under the optimal conditions, the lipid yield of microorganisms was 1.81 g/L and the carbon–conversion ratio reached 82.53% while lipid yield and the carbon–conversion ratio in a monoculture fell in the range of 0.79–0.81 g/L and 55.93–62.61%, respectively. Therefore, compared to the monoculture model, the co-fermentation of Chlorella vulgaris and Rhodotorula glutinis in starch processing effluent could convert nutrients to single-cell oil in a more efficient way. It should be noted that with the reduced concentration of residual organic carbon in effluent and the increased carbon–conversion ratio, co-fermentation of microalgae and yeast can be regarded as a promising and applicable strategy for starch processing effluent remediation and low-cost biofuel feedstock production.

/pdf/co-fermentation-of-chlorella-vulgaris-with-oleaginous-yeast-1kziypr4.pdf

Co-Fermentation of Chlorella vulgaris with Oleaginous Yeast in Starch Processing Effluent as a Carbon-Reducing Strategy for Wastewater Treatment and Biofuel Feedstock Production

Systemic lupus erythematosus (SLE) is a complex autoimmune disease with a variety of clinical manifestations. Although inter-individual variations exist with respect to susceptibility to develop SLE, no study has been carried out to determine the role of different climate conditions in predisposing the susceptible individuals to SLE. The objective of this study was to investigate the role of different seasons and climate factors on SLE activity. From 2000 to 2009, the seasonal distribution of 2,802 active SLE patients recruited from Anhui Provincial Hospital and the First Affiliated Hospital of Anhui Medical University was analyzed retrospectively. The climate data were provided by the Institute of Geographical Sciences and Resources, Chinese Academy of Sciences. The correlation between climate factors and SLE activity was also analyzed. The proportion of active SLE patients in winter, spring, summer, and autumn was 10.06, 10.31, 9.74, and 8.66‰, respectively. In autumn, the proportion was much lower than that in winter and spring (P 0.05). The number of active SLE patients had no correlation with air temperature (r = 0.483, P > 0.05), relative humidity (r = -0.294, P > 0.05), and sunshine percentage (r = 0.503, P > 0.05), but it had positive correlation with amount of precipitation (r = 0.601, P < 0.05), wind velocity (r = 0.713, P < 0.01), and sunshine duration (r = 0.769, P < 0.01) and negative correlation with barometric pressure (r = -0.664, P < 0.05). The disease activity of patients with SLE is affected by seasons and climate factors.

Seasonal distribution of systemic lupus erythematosus activity and its correlation with climate factors

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Papers

MicroRNA-101, mitogen-activated protein kinases and mitogen-activated protein kinases phosphatase-1 in systemic lupus erythematosus.

Sex-specific differences in the relationship between the single-nucleotide polymorphism rs2298804 of FCER1A and the susceptibility to systemic lupus erythematosus in a Chinese Han population.

Association study between the TP53 Rs1042522G/C polymorphism and susceptibility to systemic lupus erythematosus in a Chinese Han population.

Co-Fermentation of Chlorella vulgaris with Oleaginous Yeast in Starch Processing Effluent as a Carbon-Reducing Strategy for Wastewater Treatment and Biofuel Feedstock Production

Seasonal distribution of systemic lupus erythematosus activity and its correlation with climate factors