Duodenal mucosa of untreated celiac disease patients has altered expression of the GAS6 and PROS1 and the negative regulator tyrosine kinase TAM receptors subfamily

Copyright © 2024. Published by Elsevier Inc.

Bibliographische Detailangaben
Veröffentlicht in:Clinical immunology (Orlando, Fla.). - 1999. - 263(2024) vom: 21. Juni, Seite 110202
1. Verfasser: Perez, Federico (VerfasserIn)
Weitere Verfasser: Iribarren, María Luz, Olexen, Cinthia Mariel, Ruera, Carolina Naymé, Errasti, Andrea Emilse, Guzman, Luciana, Garbi, Laura, Carrera Silva, Eugenio Antonio, Chirdo, Fernando Gabriel
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2024
Zugriff auf das übergeordnete Werk:Clinical immunology (Orlando, Fla.)
Schlagworte:Journal Article Celiac disease GAS6 Inflammation Interferons PROS1 Small intestine TAM receptors AXL protein, human Axl Receptor Tyrosine Kinase mehr... c-Mer Tyrosine Kinase EC 2.7.10.1 growth arrest-specific protein 6 Intercellular Signaling Peptides and Proteins 9008-11-1 MERTK protein, human PROS1 protein, human Protein S Proto-Oncogene Proteins Receptor Protein-Tyrosine Kinases TYRO3 protein, human
Beschreibung
Zusammenfassung:Copyright © 2024. Published by Elsevier Inc.
Celiac disease (CD) is an immune-driven disease characterized by tissue damage in the small intestine of genetically-susceptible individuals. We evaluated here a crucial immune regulatory pathway involving TYRO3, AXL, and MERTK (TAM) receptors and their ligands PROS1 and GAS6 in duodenal biopsies of controls and CD patients. We found increased GAS6 expression associated with downregulation of PROS1 and variable TAM receptors levels in duodenum tissue of CD patients. Interestingly, CD3+ lymphocytes, CD68+, CD11c+ myeloid and epithelial cells, showed differential expressions of TAM components comparing CD vs controls. Principal component analysis revealed a clear segregation of two groups of CD patients based on TAM components and IFN signaling. In vitro validation demonstrated that monocytes, T lymphocytes and epithelial cells upregulated TAM components in response to IFN stimulation. Our findings highlight a dysregulated TAM axis in CD related to IFN signaling and contribute to a deeper understanding of the pathophysiology of CD
Beschreibung:Date Completed 17.05.2024
Date Revised 22.08.2024
published: Print-Electronic
Citation Status MEDLINE
ISSN:1521-7035
DOI:10.1016/j.clim.2024.110202