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MAPK4 inhibits the early aberrant activation of B cells in rheumatoid arthritis by promoting the IRF4-SHIP1 signaling pathway.
Cell Death Dis
January 2025
Department of Pediatrics, Affiliated Hospital of Zunyi Medical University, Zunyi, China.
The involvement of B lymphocytes in the pathogenesis of rheumatoid arthritis (RA) is well-established, with their early and aberrant activation being a crucial factor. However, the mechanisms underlying this abnormal activation in RA remain incompletely understood. In this study, we identified a significant reduction in MAPK4 expression in both RA patients and collagen-induced arthritis (CIA) mouse models, which correlates with disrupted B cell activation.
View Article and Find Full Text PDFChordoma Spontaneous Regression After COVID-19.
Viruses
December 2024
University Hospital of UFMA, Federal University of Maranhao, São Luís 65080-805, Maranhão, Brazil.
Chordomas are a low-to-intermediate-grade slow-growing subtype of sarcoma, but show propensity to grow and invade locally with recurrence and metastasis in 10-40% of cases. We describe the first case of spontaneous regression of a solid tumor (histologically and immunohistochemically proven chordoma) after COVID-19. A female patient with clival chordoma underwent occipitocervical fixation prior to tumor resection.
View Article and Find Full Text PDFCeliac Disease: A Transitional Point of View.
Nutrients
January 2025
Clinical Immunology Outpatient Clinic, Division of Internal Medicine, Department of Advanced Medical and Surgical Sciences, "Luigi Vanvitelli" University of Campania, 80131 Naples, Italy.
Celiac disease (CeD) is a chronic, lifelong, multifactorial, polygenic, and autoimmune disorder, characteristically triggered by exposure to the exogenous factor "gluten" in genetically predisposed individuals, with resulting duodenal inflammation and enteropathy, as well as heterogeneous multisystemic and extraintestinal manifestations. The immunopathogenesis of CeD is complex, favored by a peculiar human leukocyte antigen (HLA) genetic predisposition, leading to gluten presentation by antigen-presenting cells to CD4+ T helper (Th) cells, T cell-B cell interactions, and production of specific antibodies, resulting in the immune-mediated killing of enterocytes and, macroscopically, in duodenal inflammation. Here, the most relevant correlations between cellular and molecular aspects and clinical manifestations of this complex disease are reviewed, with final considerations on nutritional aspects for disease management.
View Article and Find Full Text PDFExploring CAR T-Cell Dynamics: Balancing Potent Cytotoxicity and Controlled Inflammation in CAR T-Cells Derived from Systemic Sclerosis and Myositis Patients.
Int J Mol Sci
January 2025
Department of Internal Medicine 5, Hematology and Oncology, Friedrich-Alexander-Universität Erlangen-Nürnberg and Universitätsklinikum Erlangen, 91054 Erlangen, Germany.
Systemic lupus erythematosus (SLE), systemic sclerosis (SSc), and idiopathic inflammatory myositis (IIM) are autoimmune diseases managed with long-term immunosuppressive therapies. Hu19-CD828Z, a fully human anti-CD19 chimeric antigen receptor (CAR) with a CD28 costimulatory domain, is engineered to potently deplete B-cells. In this study, we manufactured Hu19-CD828Z CAR T-cells from peripheral blood of SLE, IIM, and SSc patients and healthy donors (HDs).
View Article and Find Full Text PDFTargeting NF-kappaB-inducing kinase shapes B-cell homeostasis in myasthenia gravis.
J Neuroinflammation
January 2025
Department of Neurology, Affiliated Hospital of Xuzhou Medical University, No. 99 Huaihai West Road, Quanshan District, Xuzhou, Jiangsu, China.
Background: B cell immune dysregulation plays a critical role in myasthenia gravis (MG). However, targeted B-cell therapy such as rituximab may result in long-term peripheral B cell clearance and allow for the survival of plasma cells, contributing to frequent infections and relapses. Therefore, we aimed to identify potential novel therapeutic targets that preserve part of B cell function while inhibiting antibody-secreting cells (ASCs).
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