Systemic Lupus Erythematosus: Definitions, Contexts, Conflicts, Enigmas

Rekvig, Ole Petter

doi:10.3389/fimmu.2018.00387

Cited by 38 publications

(74 citation statements)

References 160 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with several clinical manifestations and immunological alteration [1]. The interaction of sex, environmental factors, and hormonal status, including especially the hypothalamo-pituitary-adrenal axis (HPA) alteration, contribute to the development and existing of the disease.…”

Section: Discussionmentioning

confidence: 99%

“…The interaction of sex, environmental factors, and hormonal status, including especially the hypothalamo-pituitary-adrenal axis (HPA) alteration, contribute to the development and existing of the disease. SLE is characterised by the loss of immune tolerance, aberrations of communication, differentiation, and activation of immune cells and pathways [1,2]. Besides regulating metabolism, blood pressure, inflammation, and many other processes, changes in the cortisol level influence the cognitive function, the behaviour, and the reaction to stress [14].…”

Section: Discussionmentioning

confidence: 99%

“…Systemic lupus erythematosus (SLE) is a chronic, autoimmune disease which can damage many organs [1]. Despite of the survival of SLE patients has improved over the last 50 years, owing to the innovative therapies, the most appropriate scheme is absent.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Polymorphisms of human glucocorticoid receptor gene in systemic lupus erythematosus: a single-centre result

et al. 2019

View full text Add to dashboard Cite

Background SLE is a systemic autoimmune disorder with multiple organ manifestations. Despite of the innovations glucocorticoids (GC) have still remained the first-line therapy in SLE. Besides HSD11B enzymes, intracellular glucocorticoid receptors (GR) affect tissue-specific cortisol effect and the consequent signalisation pathway. SNPs of the glucocorticoid receptor gene (NR3C1) modulate individual sensitivity to glucocorticoids. Our aim was to determine the allele frequency of the three, clinically most important SNPs in a SLE patient population in comparison to healthy volunteers and to find association with particular manifestations of SLE. Methods We analysed results of 104 SLE patients compared to 160 healthy subjects. All patients were genotyped for the functional GR polymorphisms BclI, N363S, and A3669G. The GR gene polymorphisms were determined using allele-specific PCR and Taqman allelic discrimination assays. Results The BclI allele frequency was lower in the SLE group compared to the healthy control group. The central nervous system and especially psychiatric symptoms developed more frequently in the BclI carriers compared to none carriers. The prevalence of theA3669G polymorphism was the same in both groups, but showed a negative association with the psychiatric symptoms. Conclusion The increased and decreased sensitivity associated with GR BclI and A3669G polymorphisms could have a pathogenic significance in SLE especial with the central nervous system and psychiatric symptoms. Improving our knowledge on the importance of GR polymorphisms may reveal their pathophysiologic and therapeutic consequences.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Polymorphisms of human glucocorticoid receptor gene in systemic lupus erythematosus: a single-centre result

et al. 2019

View full text Add to dashboard Cite

show abstract

“…In the introduction to the revised SLICC SLE classification criteria it is stated “ To ensure that there is a consistent definition of SLE for the purposes of research and surveillance, classification criteria for SLE are needed ” ( 2 ). This statement indicates that the ACR or SLICC classification criteria are valid as reliable approaches to define SLE, even though they do not define SLE as a homogenous disease since the classification criteria by definition provides hundreds of clinical phenotypes [discussed in ( 3 )]. Figure 1 principally demonstrates the clinical phenotype variability problem.…”

Section: Introductionmentioning

confidence: 99%

Autoimmunity and SLE: Factual and Semantic Evidence-Based Critical Analyses of Definitions, Etiology, and Pathogenesis

Rekvig

2020

Front. Immunol.

Self Cite

View full text Add to dashboard Cite

One cannot discuss anti-dsDNA antibodies and lupus nephritis without discussing the nature of Systemic lupus erythematosus (SLE). SLE is insistently described as a prototype autoimmune syndrome, with anti-dsDNA antibodies as a central biomarker and a pathogenic factor. The two entities, “SLE” and “The Anti-dsDNA Antibody,” have been linked in previous and contemporary studies although serious criticism to this mutual linkage have been raised: Anti-dsDNA antibodies were first described in bacterial infections and not in SLE; later in SLE, viral and parasitic infections and in malignancies. An increasing number of studies on classification criteria for SLE have been published in the aftermath of the canonical 1982 American College of Rheumatology SLE classification sets of criteria. Considering these studies, it is surprising to observe a nearby complete absence of fundamental critical/theoretical discussions aimed to explain how and why the classification criteria are linked in context of etiology, pathogenicity, or biology. This study is an attempt to prioritize critical comments on the contemporary definition and classification of SLE and of anti-dsDNA antibodies in context of lupus nephritis. Epidemiology, etiology, pathogenesis, and measures of therapy efficacy are implemented as problems in the present discussion. In order to understand whether or not disparate clinical SLE phenotypes are useful to determine its basic biological processes accounting for the syndrome is problematic. A central problem is discussed on whether the clinical role of anti-dsDNA antibodies from principal reasons can be accepted as a biomarker for SLE without clarifying what we define as an anti-dsDNA antibody, and in which biologic contexts the antibodies appear. In sum, this study is an attempt to bring to the forum critical comments on the contemporary definition and classification of SLE, lupus nephritis and anti-dsDNA antibodies. Four concise hypotheses are suggested for future science at the end of this analytical study.

show abstract

“…Systemic lupus erythematosus (SLE), a chronic inflammatory disease characterized by multiple immunologic abnormalities, can damage many organs [1]. The prevalence rates of SLE are about 17-48/100,000 population worldwide, and females are 3-6 times more frequently affected than males.…”

Section: Introductionmentioning

confidence: 99%

Interaction of miR-181b and IFNA1 Polymorphisms on the Risk of Systemic Lupus Erythematosus

Yang

Zeng

Shi

2020

BioMed Research International

View full text Add to dashboard Cite

Introduction. A previous work has discovered that chromosome 1q32 locus linked to the risk of systemic lupus erythematosus (SLE) and miR-181b located on the susceptibility site with downregulation inversely correlating to its target molecular interferon alpha 1 (IFNA1). The purpose of this study was to investigate the association of miR-181b and IFNA1 polymorphisms with IS risk. Methods. The miR-181b rs322931, IFNA1 rs1332190, and rs10811543 were genotyped using a Multiplex SNaPshot assay. miR-181b expression levels in plasma of SLE patients and controls were analyzed using quantitative PCR. Results. The rs322931 CT, CT/TT, and T allele exerted an increased trend of SLE risk (CT vs. CC: adjusted OR=1.71, 95% CI 1.16-2.50, P=0.01; CT/TT vs. CC: adjusted OR=1.45, 95% CI 1.08-1.95, P=0.01; T vs. C: adjusted OR=1.38, 95% CI 1.07-1.79, P=0.01). Combined genotypes of the rs322931 CT/TT+rs1332190 TT and the rs322931 CC+rs10811543 AG/AA also revealed an increased risk of SLE. Gene-gene interaction analysis showed that a three-locus model consisting of rs322931, rs1332190, and rs10811543 attributed an increased risk of SLE. Further genotype-phenotype analysis revealed that rs322931 CT/TT carriers displayed lower levels of miR-181b. Conclusions. These findings indicate that the miR-181b rs322931 may be singly and jointly responsible for the etiology of SLE by altering miR-181b expression.

show abstract

Systemic Lupus Erythematosus: Definitions, Contexts, Conflicts, Enigmas

Cited by 38 publications

References 160 publications

Polymorphisms of human glucocorticoid receptor gene in systemic lupus erythematosus: a single-centre result

Polymorphisms of human glucocorticoid receptor gene in systemic lupus erythematosus: a single-centre result

Autoimmunity and SLE: Factual and Semantic Evidence-Based Critical Analyses of Definitions, Etiology, and Pathogenesis

Interaction of miR-181b and IFNA1 Polymorphisms on the Risk of Systemic Lupus Erythematosus

Contact Info

Product

Resources

About