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Systemic Lupus Erythematosus - PubMed

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Last Updated: 27 July 2022

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Integrative analysis of omics summary data reveals putative mechanisms linked to different cell populations in systemic lupus erythematosus.

Systemic lupus erythematosus is a multi-systemic disease with multiple interactions at the molecular level, the full details of which are uncertain. In SLE, the first step was to use TWMR to identify causal genes and causal methylation sites. We found two mediating options for SLE: 1 transcription mediation model and 2 epigenetic mediation model. SLE gene expression in various cell populations is of utmost importance in determining disease heterogeneity in various cell populations.

Source link: https://doi.org/10.1016/j.ygeno.2022.110435


Abnormal lower expression of GPR183 in peripheral blood T and B cell subsets of systemic lupus erythematosus patients.

In T cell-dependent antibody responses, a G protein-coupled receptor 183 has been shown to mediate migration and localization of immune cells. There has been no systematic investigation into the presence of GPR183 in lymphocyte subsets of SLE patients. GPR183 expression levels in over peripheral blood lymphocyte subsets of patients with SLE were reduced overall, relative to healthy controls. The difference between inactive and active SLE patients indicates that GPR183 expression between inactive and active SLE patients indicates that GPR183 expression may be concerned about SLE's disease activity. Further receiver operating characteristic curve analysis revealed that GPR183 expression in circulating CD27-IgD+ B cells could be helpful in distinguishing between active and active SLE patients. In addition, type I interferon stimulation may down-regulate the expression of GPR183 in peripheral blood T and B cell subsets.

Source link: https://doi.org/10.1080/08916934.2022.2103119


Pregnancy-related complications in systemic lupus erythematosus.

Systemic lupus erythematosus is a systemic autoimmune disease that mainly affects women of childbearing age and has resulted in various adverse pregnancy outcomes. Because of unstable disease outbreaks during the gestation period, elevated thrombosis risk, severe organ damage, and predictable side effects of immunosuppressive agents, patients with SLE were formerly discouraged. Preconception therapy, strict surveillance, and improved therapy with minimized risks for both the mother and the foetus have all been successful in SLE patients. However, pregnant women with SLE have a high risk of APOs such as disease flare, preterm birth, intrauterine growth restriction, preeclampsia, and pregnancy loss. Therefore, this report briefly explores the relationship between pregnancy outcomes and SLE, helps clarify pathophysiological and immunological changes during SLE pregnancy.

Source link: https://doi.org/10.1016/j.jaut.2022.102864


Autoantibodies in systemic lupus erythematosus: From immunopathology to therapeutic target.

Our analysis of autoreactive B cells and the pathogenic autoantibodies has been enhanced by single cell analysis of autoreactive B cells and monoclonal antibody screening from patients with active SLE. While B cell depletion therapies have been widely studied in the clinics, the development of more specific drugs against the pathogenic B cell subtype and autoantibodies has posed a major obstacle, with improved efficiency and safety still to be explored.

Source link: https://doi.org/10.1016/j.jaut.2022.102861


Abnormalities of T cells in systemic lupus erythematosus: new insights in pathogenesis and therapeutic strategies.

Multiple and persistent T cell abnormalities in SLE are intertwined with disease gene expression. In major CD4+ T helper cell subsets including Th1, Th17, regulatory, and follicular helper cells, both numerical and functional disturbances have been reported. B cells are known to be aided by IL-17 production, but insufficient IL-2 is present, and infiltrate tissues are known. In T cells from lupus prone mice and patients with SLE, all key metabolic pathways, including glycolysis, glutaminolysis, and oxidative phosphorylation have been altered, including glycolysis, glutaminolysis, and oxidative phosphorylation. T cells from SLE's CD8+ cytotoxic T cells have reduced cytolytic activity, which may be responsible for increased rates of infection and autoimmunity. In addition, CD8+ T cells in the context of rheumatic diseases lack the expression of CD8, while CD8+ T cells in the context of autoimmune disorders lack CD8+, CD8+ and infiltrate tissues. Novel approaches to eliminate these aberrations in T cells have shown promise for SLE therapy.

Source link: https://doi.org/10.1016/j.jaut.2022.102870


Brain abscess caused by Scedosporium boydii in a systemic lupus erythematosus patient: A case report and literature review.

Diagnosis and treatment of Scedosporium infections can be difficult, and the result is often fatal, particularly in patients with disseminated infections. Systemic lupus erythematosus patients have a rare case of brain absces caused by S. boydii in a systemic lupus erythematosus patient. This case demonstrates the importance of mNGS in early diagnosis of S. boydii.

Source link: https://doi.org/10.1016/j.ijmmb.2022.06.010

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions