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240405s2024 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2024.110202
|2 doi
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|a pubmed24n1509.xml
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|a (DE-627)NLM370644603
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|a (NLM)38575045
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|a (PII)S1521-6616(24)00093-7
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|a DE-627
|b ger
|c DE-627
|e rakwb
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|a eng
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|a Perez, Federico
|e verfasserin
|4 aut
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|a Duodenal mucosa of untreated celiac disease patients has altered expression of the GAS6 and PROS1 and the negative regulator tyrosine kinase TAM receptors subfamily
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|c 2024
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|a Text
|b txt
|2 rdacontent
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|a ƒaComputermedien
|b c
|2 rdamedia
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|a ƒa Online-Ressource
|b cr
|2 rdacarrier
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|a Date Completed 17.05.2024
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|a Date Revised 22.08.2024
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a Copyright © 2024. Published by Elsevier Inc.
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|a 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
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|a Journal Article
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|a Celiac disease
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|a GAS6
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|a Inflammation
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|a Interferons
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|a PROS1
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|a Small intestine
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|a TAM receptors
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|a AXL protein, human
|2 NLM
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|a Axl Receptor Tyrosine Kinase
|2 NLM
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|a c-Mer Tyrosine Kinase
|2 NLM
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|a EC 2.7.10.1
|2 NLM
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|a growth arrest-specific protein 6
|2 NLM
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|a Intercellular Signaling Peptides and Proteins
|2 NLM
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|a Interferons
|2 NLM
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|a 9008-11-1
|2 NLM
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|a MERTK protein, human
|2 NLM
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|a EC 2.7.10.1
|2 NLM
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|a PROS1 protein, human
|2 NLM
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|a Protein S
|2 NLM
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|a Proto-Oncogene Proteins
|2 NLM
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|a Receptor Protein-Tyrosine Kinases
|2 NLM
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|a EC 2.7.10.1
|2 NLM
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|a TYRO3 protein, human
|2 NLM
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|a EC 2.7.10.1
|2 NLM
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|a Iribarren, María Luz
|e verfasserin
|4 aut
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|a Olexen, Cinthia Mariel
|e verfasserin
|4 aut
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|a Ruera, Carolina Naymé
|e verfasserin
|4 aut
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|a Errasti, Andrea Emilse
|e verfasserin
|4 aut
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|a Guzman, Luciana
|e verfasserin
|4 aut
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|a Garbi, Laura
|e verfasserin
|4 aut
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|a Carrera Silva, Eugenio Antonio
|e verfasserin
|4 aut
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|a Chirdo, Fernando Gabriel
|e verfasserin
|4 aut
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0 |
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|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 263(2024) vom: 21. Juni, Seite 110202
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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|g volume:263
|g year:2024
|g day:21
|g month:06
|g pages:110202
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|u http://dx.doi.org/10.1016/j.clim.2024.110202
|3 Volltext
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|a GBV_ILN_24
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|a GBV_ILN_350
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|a AR
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|d 263
|j 2024
|b 21
|c 06
|h 110202
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