Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1111/j.1532-5415.2008.01866.x | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Association of uveitis with pediatric autoimmune diseases based on a TriNetX study.
Sci Rep
December 2024
Department of Ophthalmology, China Medical University Hospital, China Medical University, Taichung, Taiwan.
To investigate for the risk of uveitis among such patients. A retrospective cohort study utilized the TriNetX database and recruited pediatric autoimmune patients diagnosed between January 1st 2004 and December 31st 2022. The non-autoimmune cohort were randomly selected control patients matched by sex, age, and index year.
View Article and Find Full Text PDFNET formation-mediated in situ protein delivery to the inflamed central nervous system.
Nat Commun
December 2024
College of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul, Republic of Korea.
Delivering protein drugs to the central nervous system (CNS) is challenging due to the blood-brain and blood-spinal cord barrier. Here we show that neutrophils, which naturally migrate through these barriers to inflamed CNS sites and release neutrophil extracellular traps (NETs), can be leveraged for therapeutic delivery. Tannic acid nanoparticles tethered with anti-Ly6G antibody and interferon-β (aLy6G-IFNβ@TLP) are constructed for targeted neutrophil delivery.
View Article and Find Full Text PDFJAK inhibition decreases the autoimmune burden in Down syndrome.
Elife
December 2024
Linda Crnic Institute for Down Syndrome, University of Colorado Anschutz Medical Campus, Aurora, United States.
Background: Individuals with Down syndrome (DS), the genetic condition caused by trisomy 21 (T21), display clear signs of immune dysregulation, including high rates of autoimmunity and severe complications from infections. Although it is well established that T21 causes increased interferon responses and JAK/STAT signaling, elevated autoantibodies, global immune remodeling, and hypercytokinemia, the interplay between these processes, the clinical manifestations of DS, and potential therapeutic interventions remain ill defined.
Methods: We report a comprehensive analysis of immune dysregulation at the clinical, cellular, and molecular level in hundreds of individuals with DS, including autoantibody profiling, cytokine analysis, and deep immune mapping.
Unraveling 's biofunction in human disease.
Front Oncol
December 2024
The Affiliated Lihuili Hospital of Ningbo University, Ningbo, China.
Interferon-induced protein 44-like () is regarded as an immune-related gene and is a member of interferon-stimulated genes (ISGs). They participate in network transduction, and its own epigenetic modifications, apoptosis, cell-matrix formation, and many other pathways in tumors, autoimmune diseases, and viral infections. The current review provides a comprehensive overview of the onset and biological mechanisms of and its potential clinical applications in malignant tumors and non-neoplastic diseases.
View Article and Find Full Text PDFSuccessful Management of Severe and Refractory Autoimmune Hemolytic Anemia (AIHA) in a Sickle Cell Disease Patient With Bortezomib.
Cureus
November 2024
Hematology and Medical Oncology, Al-Zahraa Medical College, Basrah, IRQ.
Autoimmune hemolytic anemia (AIHA) is a multifactorial disease that causes immune-mediated red blood cell destruction, resulting in anemia and hemolysis symptoms. Despite a significant understanding of its pathogenesis, the precise causes of AIHA remain largely unclear and are thought to be multifactorial. In this paper, we presented a case of sickle cell anemia who developed severe AIHA that failed to maintain response to multiple treatment lines, including steroids, intravenous immunoglobulin, rituximab, and immune suppressive medications.
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!