Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9413775 | PMC |
| http://dx.doi.org/10.2340/00015555-3865 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Role of STING Deficiency in Amelioration of Mouse Models of Lupus and Atherosclerosis.
Arthritis Rheumatol
November 2024
National Institute of Arthritis and Musculoskeletal and Skin Diseases, NIH, Bethesda, Maryland.
Objective: Systemic lupus erythematosus (SLE) is a systemic autoimmune syndrome characterized by autoreactive responses to nucleic acids, dysregulation of the type I interferon (IFN-I) pathway, and accelerated atherosclerosis. The stimulator of IFN genes (STING), a cytosolic DNA sensor, has pathogenic implications in various inflammatory diseases. However, its specific role in SLE pathogenesis, particularly in tissue damage, remains unclear.
View Article and Find Full Text PDFManifestations of Hydralazine-Induced Vasculitis: A Case Series.
Cureus
October 2024
Internal Medicine, Northeast Georgia Medical Center Gainesville, Gainesville, USA.
Article Synopsis
- Hydralazine has been used for many years to treat high blood pressure, but it can cause serious side effects, including autoimmune diseases like ANCA-vasculitis and a lupus-like syndrome.
- The text discusses four cases of vasculitis linked to hydralazine, showing varying symptoms like lung hemorrhage, coughing up blood, and skin rashes.
- Diagnosing these conditions can be challenging, often requiring kidney biopsy, and the treatment involves stopping hydralazine and using immunosuppressants; caution is advised in using hydralazine over other blood pressure medications.
A rare cause of immune dysregulation, prolidase deficiency: a case report and review of the literature.
Immunol Res
December 2024
Division of Pediatric Genetics, Department of Child Health and Diseases, Faculty of Medicine Hospital, Dokuz Eylul University, Izmir, Turkey.
We report a pediatric patient with prolidase deficiency, caused by a mutation in the PEPD gene, which encodes the enzyme prolidase D, with a lupus-like clinic and marked dysmorphic features along with pulmonary, neurological, skeletal, and immune system involvement. In addition to being the first known case in the literature where Friedrich's ataxia and prolidase deficiency were observed together, we aimed to highlight that this diagnosis should be considered in patients with autoimmunity and additional systemic findings such as treatment-resistant skin lesions, intellectual disability, and pulmonary manifestations. Furthermore, we sought to compare this case with others documented in the literature.
View Article and Find Full Text PDFDeletion of the Mitochondrial Membrane Protein Fam210b Is Associated with the Development of Systemic Lupus Erythematosus.
Int J Mol Sci
July 2024
Beijing Institute of Brain Disorders, Laboratory of Brain Disorders, Ministry of Science and Technology, Collaborative Innovation Center for Brain Disorders, Capital Medical University, No. 10 Xitoutiao, You An Men, Beijing 100069, China.
Mitochondrial dysfunction has been increasingly recognized as a trigger for systemic lupus erythematosus (SLE). Recent bioinformatics studies have suggested Fam210b as a significant candidate for the classification and therapeutic targeting of SLE. To experimentally prove the role of Fam210b in SLE, we constructed knockout () mice using the CRISPR-Cas9 method.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!