Systemic lupus erythematosus (SLE) is a typical systemic autoimmune disease that manifests as skin rash, arthritis, lymphadenopathy, and multiple organ lesions. Epigenetics, including DNA methylation, histone modification, and non-coding RNA regulation, mainly affect the function and characteristics of cells through the regulation of gene transcription or translation. Increasing evidence indicates that there are a variety of complex epigenetic effects in patients with SLE, which interfere with the differentiation and function of T, and B lymphocytes, monocytes, and neutrophils, and enhance the expression of SLE-associated pathogenic genes. This paper summarizes our currently knowledge regarding pathogenesis of SLE, and introduces current advances in the epigenetic regulation of SLE from three aspects: immune function, inflammatory response, and lupus complications. We propose that epigenetic changes could be used as potential biomarkers and therapeutic targets of SLE.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/j.clim.2023.109857 | DOI Listing |
Clin Rheumatol
January 2025
Department of Rheumatology and Immunology, Peking University People's Hospital, 11 Xizhimen South Street, Beijing, 100044, China.
Objective: To investigate the dose effect of methylprednisolone (MP) on peripheral lymphocyte profiles in patients with systemic lupus erythematosus (SLE). This study investigated the impact of varied MP doses on peripheral lymphocyte subtypes in SLE patients.
Methods: We conducted a prospective study involving 51 SLE patients, categorized into four groups (40 mg/day, 80 mg/day, 500 mg/day, and 1000 mg/day) based on the administered MP dosage during hospitalization.
Cureus
December 2024
Pain Medicine, Fondazione Paolo Procacci, Rome, ITA.
Systemic lupus erythematosus (SLE) is an autoimmune disease that more commonly affects African American people, although it is seen in people of all racial backgrounds. This condition is characterized by a dysregulated immune response resulting in widespread inflammation. Clinical manifestations caused by this inflammation include arthritis, anemia, cutaneous rashes, pleuritis, and nephritis.
View Article and Find Full Text PDFSAGE Open Med Case Rep
January 2025
Division of Dermatology, Faculty of Medicine, University of Ottawa, Ottawa, ON, Canada.
Discoid lupus erythematosus is a chronic, recurring, autoimmune skin disease causing annular, scarring plaques on the head and neck. Deucravacitinib, a tyrosine kinase 2 inhibitor in the Janus kinase inhibitor family, represents an emerging treatment option in systemic lupus erythematosus with potential applicability to discoid lupus erythematosus. We describe a 48-year-old woman with multiple treatment-refractory scalp plaques and associated alopecia treated with deucravacitinib.
View Article and Find Full Text PDFBMC Med
January 2025
Department of Rheumatology, Peking Union Medical College Hospital (PUMCH), Peking Union Medical College and Chinese Academy of Medical Sciences, National Clinical Research Center for Dermatologic and Immunologic Diseases (NCRC-DID), Key Laboratory of Rheumatology and Clinical Immunology, Ministry of Education, No. 1 Shuaifuyuan, Wangfujing Ave, Beijing, 100730, China.
Background: Patients with systemic lupus erythematosus (SLE) suffered from an increasing risk of cardiovascular diseases. In this multi-center prospective study, we aimed to determine the association between antiphospholipid antibodies (aPLs) and future atherosclerotic cardiovascular disease (ASCVD) in SLE.
Methods: In total, 1573 SLE patients were recruited based on the Chinese SLE Treatment and Research group (CSTAR) registry.
RMD Open
January 2025
Assistance Publique-Hôpitaux de Paris (AP-HP), Groupement Hospitalier Pitié-Salpêtrière, Centre de Référence des maladies auto-immunes et auto-inflammatoires systémiques rares de l'adulte d'Ile-de-France, Centre et Martinique, Service de Médecine Interne 2, Institut E3M, Paris, France, paris, France.
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!