LIVIVO - Search results -

Search results

Result 1 - 10 of total 31

Search options

Article ; Online: IFN-I inducible

Vuillier, Françoise / Li, Zhi / Black, Iain / Cruciani, Melania / Rubino, Erminia / Michel, Frédérique / Pellegrini, Sandra

Frontiers in immunology

2022 Volume 13, Page(s) 939907

Abstract: Regulation of innate immune responses is essential for maintenance of immune homeostasis and development of an appropriate immunity against microbial infection. We show here ... ...

Abstract	Regulation of innate immune responses is essential for maintenance of immune homeostasis and development of an appropriate immunity against microbial infection. We show here that
MeSH term(s)	Adenosine Deaminase/metabolism ; Antibodies ; Antiviral Agents ; HeLa Cells ; Humans ; Immunity, Innate ; Interferon Type I ; MicroRNAs/genetics ; Protein Isoforms ; RNA, Double-Stranded ; RNA-Binding Proteins/metabolism ; Transcription Factors/genetics ; Tripartite Motif Proteins/genetics ; Ubiquitin-Protein Ligases/genetics
Chemical Substances	Antibodies ; Antiviral Agents ; Interferon Type I ; MicroRNAs ; Protein Isoforms ; RNA, Double-Stranded ; RNA-Binding Proteins ; Transcription Factors ; Tripartite Motif Proteins ; TRIM25 protein, human (EC 2.3.2.27) ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; ADAR protein, human (EC 3.5.4.37) ; Adenosine Deaminase (EC 3.5.4.4)
Language	English
Publishing date	2022-07-22
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2022.939907
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Article ; Online: Two common disease-associated TYK2 variants impact exon splicing and TYK2 dosage.

Li, Zhi / Rotival, Maxime / Patin, Etienne / Michel, Frédérique / Pellegrini, Sandra

PloS one

2020 Volume 15, Issue 1, Page(s) e0225289

Abstract: TYK2 belongs to the JAK protein tyrosine kinase family and mediates signaling of numerous antiviral and immunoregulatory cytokines (type I and type III IFNs, IL-10, IL-12, IL-22, IL-23) in immune and non-immune cells. After many years of genetic ... ...

Abstract	TYK2 belongs to the JAK protein tyrosine kinase family and mediates signaling of numerous antiviral and immunoregulatory cytokines (type I and type III IFNs, IL-10, IL-12, IL-22, IL-23) in immune and non-immune cells. After many years of genetic association studies, TYK2 is recognized as a susceptibility gene for some inflammatory and autoimmune diseases (AID). Seven TYK2 variants have been associated with AIDs in Europeans, and establishing their causality remains challenging. Previous work showed that a protective variant (P1104A) is hypomorphic and also a risk allele for mycobacterial infection. Here, we have studied two AID-associated common TYK2 variants: rs12720270 located in intron 7 and rs2304256, a non-synonymous variant in exon 8 that causes a valine to phenylalanine substitution (c.1084 G > T, Val362Phe). We found that this amino acid substitution does not alter TYK2 expression, catalytic activity or ability to relay signaling in EBV-B cell lines or in reconstituted TYK2-null cells. Based on in silico predictions that these variants may impact splicing of exon 8, we: i) analyzed TYK2 transcripts in genotyped EBV-B cells and in CRISPR/Cas9-edited cells, ii) measured splicing using minigene assays, and iii) performed eQTL (expression quantitative trait locus) analysis of TYK2 transcripts in primary monocytes and whole blood cells. Our results reveal that the two variants promote the inclusion of exon 8, which, we demonstrate, is essential for TYK2 binding to cognate receptors. In addition and in line with GTEx (Genetic Tissue Expression) data, our eQTL results show that rs2304256 mildly enhances TYK2 expression in whole blood. In all, these findings suggest that these TYK2 variants are not neutral but instead have a potential impact in AID.
MeSH term(s)	Alleles ; Amino Acid Substitution/genetics ; Autoimmune Diseases/blood ; Autoimmune Diseases/genetics ; Autoimmune Diseases/pathology ; B-Lymphocytes/metabolism ; B-Lymphocytes/pathology ; Cytokines/chemistry ; Cytokines/genetics ; Gene Expression Regulation/genetics ; Genetic Association Studies ; Genetic Predisposition to Disease ; Genotype ; Humans ; Inflammation/blood ; Inflammation/genetics ; Inflammation/pathology ; Phenylalanine/genetics ; Polymorphism, Single Nucleotide/genetics ; Quantitative Trait Loci/genetics ; TYK2 Kinase/blood ; TYK2 Kinase/genetics
Chemical Substances	Cytokines ; Phenylalanine (47E5O17Y3R) ; TYK2 Kinase (EC 2.7.10.2) ; TYK2 protein, human (EC 2.7.10.2)
Language	English
Publishing date	2020-01-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0225289
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: Expression of endogenous retroviruses reflects increased usage of atypical enhancers in T cells.

Azébi, Saliha / Batsché, Eric / Michel, Frédérique / Kornobis, Etienne / Muchardt, Christian

The EMBO journal

2019 Volume 38, Issue 12

Abstract: Several autoimmune diseases including multiple sclerosis (MS) cause increased transcription of endogenous retroviruses (HERVs) normally repressed by heterochromatin. In parallel, HERV-derived sequences were reported to drive gene expression. Here, we ... ...

Abstract	Several autoimmune diseases including multiple sclerosis (MS) cause increased transcription of endogenous retroviruses (HERVs) normally repressed by heterochromatin. In parallel, HERV-derived sequences were reported to drive gene expression. Here, we have examined a possible link between promoter and enhancer divergent transcription and the production of HERV transcripts. We find that HERV-derived sequences are in general counter-selected at regulatory regions, a counter-selection that is strongest in brain tissues while very moderate in stem cells. By exposing T cells to the pesticide dieldrin, we further found that a series of HERV-driven enhancers otherwise active only at stem cell stages can be reactivated by stress. This in part relies on peptidylarginine deiminase activity, possibly participating in the reawakening of silenced enhancers. Likewise, usage of HERV-driven enhancers was increased in myelin-reactive T cells from patients with MS, correlating with activation of nearby genes at several sites. Altogether, we propose that HERV-driven enhancers constitute a reservoir of auxiliary enhancers transiently induced by stress while chronically active in diseases like MS.
MeSH term(s)	Adult ; Case-Control Studies ; Cells, Cultured ; Endogenous Retroviruses/genetics ; Female ; Gene Expression Regulation, Viral/physiology ; Humans ; Jurkat Cells ; Male ; Middle Aged ; Multiple Sclerosis/genetics ; Multiple Sclerosis/immunology ; Multiple Sclerosis/metabolism ; Multiple Sclerosis/virology ; Regulatory Sequences, Nucleic Acid/genetics ; T-Lymphocytes/metabolism ; T-Lymphocytes/pathology
Language	English
Publishing date	2019-05-08
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	586044-1
ISSN	1460-2075 ; 0261-4189
ISSN (online)	1460-2075
ISSN	0261-4189
DOI	10.15252/embj.2018101107
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 1808: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 100: Show issues

Order via subito

Details ▾

Article ; Online: Central Role of Macrophages and Nucleic Acid Release in Myasthenia Gravis Thymus.

Payet, Cloé A / You, Axel / Fayet, Odessa-Maud / Hemery, Edouard / Truffault, Frederique / Bondet, Vincent / Duffy, Darragh / Michel, Frédérique / Fadel, Elie / Guihaire, Julien / Demeret, Sophie / Berrih-Aknin, Sonia / Le Panse, Rozen

Annals of neurology

2023 Volume 93, Issue 4, Page(s) 643–654

Abstract: Objective: Myasthenia gravis (MG) is a neuromuscular disease mediated by antibodies against the acetylcholine receptor (AChR). The thymus plays a primary role in AChR-MG and is characterized by a type I interferon (IFN) signature linked to IFN-β. We ... ...

Abstract	Objective: Myasthenia gravis (MG) is a neuromuscular disease mediated by antibodies against the acetylcholine receptor (AChR). The thymus plays a primary role in AChR-MG and is characterized by a type I interferon (IFN) signature linked to IFN-β. We investigated if AChR-MG was characterized by an IFN-I signature in the blood, and further investigated the chronic thymic IFN-I signature. Methods: Serum levels of IFN-β and IFN-α subtypes, and mRNA expression for IFN-I subtypes and IFN-stimulated genes in peripheral mononuclear blood cells (PBMCs) were analyzed. The contribution of endogenous nucleic acids in thymic expression of IFN-I subtypes was investigated in human thymic epithelial cell cultures and the mouse thymus. By immunohistochemistry, thymic CD68 Results: No IFN-I signature was observed in the periphery emphasizing that the IFN-I signature is restricted to the MG thymus. Molecules mimicking endogenous dsDNA signalization (Poly(dA:dT) and 2'3'-cGAMP), or dexamethasone-induced necrotic thymocytes increased IFN-β and α-AChR expression by thymic epithelial cells, and in the mouse thymus. A significant decrease in thymic macrophages was demonstrated in AChR-MG. In mice, a decrease in thymic macrophages led to an increase of necrotic thymocytes associated with IFN-β and α-AChR expression. Interpretation: These results suggest that the decrease of thymic macrophages in AChR-MG impairs the elimination of apoptotic thymocytes favoring the release of endogenous nucleic acids from necrotic thymocytes. In this inflammatory context, thymic epithelial cells may overexpress IFN-β, which specifically induces α-AChR, resulting in self-sensitization and thymic changes leading to AChR-MG. ANN NEUROL 2023;93:643-654.
MeSH term(s)	Humans ; Mice ; Animals ; Nucleic Acids ; Myasthenia Gravis ; Thymus Gland/metabolism ; Receptors, Cholinergic ; Macrophages/metabolism
Chemical Substances	Nucleic Acids ; Receptors, Cholinergic
Language	English
Publishing date	2023-01-25
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80362-5
ISSN	1531-8249 ; 0364-5134
ISSN (online)	1531-8249
ISSN	0364-5134
DOI	10.1002/ana.26590
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 1370: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 478: Show issues

Order via subito

Details ▾

Article ; Online: Type I interferon-enhanced IL-10 expression in human CD4 T cells is regulated by STAT3, STAT2, and BATF transcription factors.

Govender, Umeshree / Corre, Béatrice / Bourdache, Yasmine / Pellegrini, Sandra / Michel, Frédérique

Journal of leukocyte biology

2017 Volume 101, Issue 5, Page(s) 1181–1190

Abstract: Type I IFN can exert pro- and anti-inflammatory activities in the immune system. Here, we have investigated the mechanism by which IFN-α enhances early expression of the anti-inflammatory cytokine IL-10 in human ... ...

Abstract	Type I IFN can exert pro- and anti-inflammatory activities in the immune system. Here, we have investigated the mechanism by which IFN-α enhances early expression of the anti-inflammatory cytokine IL-10 in human CD45RA
MeSH term(s)	Antibodies/pharmacology ; Basic-Leucine Zipper Transcription Factors/antagonists & inhibitors ; Basic-Leucine Zipper Transcription Factors/genetics ; Basic-Leucine Zipper Transcription Factors/immunology ; Binding Sites ; CD28 Antigens/antagonists & inhibitors ; CD28 Antigens/genetics ; CD28 Antigens/immunology ; CD3 Complex/genetics ; CD3 Complex/immunology ; CD4-Positive T-Lymphocytes/cytology ; CD4-Positive T-Lymphocytes/drug effects ; CD4-Positive T-Lymphocytes/immunology ; Cycloheximide/pharmacology ; Enhancer Elements, Genetic ; Gene Expression Regulation ; Humans ; Interferon-alpha/immunology ; Interferon-alpha/pharmacology ; Interleukin-10/genetics ; Interleukin-10/immunology ; Phosphorylation/drug effects ; Primary Cell Culture ; Protein Binding ; Protein Isoforms/genetics ; Protein Isoforms/immunology ; RNA, Small Interfering/genetics ; RNA, Small Interfering/metabolism ; STAT1 Transcription Factor/antagonists & inhibitors ; STAT1 Transcription Factor/genetics ; STAT1 Transcription Factor/immunology ; STAT2 Transcription Factor/antagonists & inhibitors ; STAT2 Transcription Factor/genetics ; STAT2 Transcription Factor/immunology ; STAT3 Transcription Factor/antagonists & inhibitors ; STAT3 Transcription Factor/genetics ; STAT3 Transcription Factor/immunology ; Signal Transduction
Chemical Substances	Antibodies ; BATF protein, human ; Basic-Leucine Zipper Transcription Factors ; CD28 Antigens ; CD3 Complex ; IL10 protein, human ; Interferon-alpha ; Protein Isoforms ; RNA, Small Interfering ; STAT1 Transcription Factor ; STAT1 protein, human ; STAT2 Transcription Factor ; STAT2 protein, human ; STAT3 Transcription Factor ; STAT3 protein, human ; Interleukin-10 (130068-27-8) ; Cycloheximide (98600C0908)
Language	English
Publishing date	2017-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	605722-6
ISSN	1938-3673 ; 0741-5400
ISSN (online)	1938-3673
ISSN	0741-5400
DOI	10.1189/jlb.2A0416-187RR
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 603: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article: Human Ubiquitin-Specific Peptidase 18 Is Regulated by microRNAs

Rubino, Erminia / Cruciani, Melania / Tchitchek, Nicolas / Le Tortorec, Anna / Rolland, Antoine D / Veli, Önay / Vallet, Leslie / Gaggi, Giulia / Michel, Frédérique / Dejucq-Rainsford, Nathalie / Pellegrini, Sandra

Frontiers in genetics

2021 Volume 11, Page(s) 627007

Abstract: Ubiquitin-specific peptidase 18 (USP18) acts as gatekeeper of type I interferon (IFN) responses by binding to the IFN receptor subunit IFNAR2 and preventing activation of the downstream JAK/STAT pathway. In any given cell type, the level of USP18 is a ... ...

Abstract	Ubiquitin-specific peptidase 18 (USP18) acts as gatekeeper of type I interferon (IFN) responses by binding to the IFN receptor subunit IFNAR2 and preventing activation of the downstream JAK/STAT pathway. In any given cell type, the level of USP18 is a key determinant of the output of IFN-stimulated transcripts. How the baseline level of USP18 is finely tuned in different cell types remains ill defined. Here, we identified microRNAs (miRNAs) that efficiently target
Language	English
Publishing date	2021-02-03
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2606823-0
ISSN	1664-8021
ISSN	1664-8021
DOI	10.3389/fgene.2020.627007
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Altered Immune Phenotypes and

Devi-Marulkar, Priyanka / Moraes-Cabe, Carolina / Campagne, Pascal / Corre, Béatrice / Meghraoui-Kheddar, Aida / Bondet, Vincent / Llibre, Alba / Duffy, Darragh / Maillart, Elisabeth / Papeix, Caroline / Pellegrini, Sandra / Michel, Frédérique

Frontiers in immunology

2021 Volume 12, Page(s) 628375

Abstract: Background: Interferon beta (IFN: Aim: To determine a combination of cellular and molecular blood signatures associated with the efficacy of IFN: Methods: The immune status of 40 RRMS patients, 15 of whom were untreated and 25 that received IFN: ...

Abstract	Background: Interferon beta (IFN Aim: To determine a combination of cellular and molecular blood signatures associated with the efficacy of IFN Methods: The immune status of 40 RRMS patients, 15 of whom were untreated and 25 that received IFN Results: Clinical responders and non-responders displayed similar plasma levels of IFN
MeSH term(s)	Adult ; CD4-Positive T-Lymphocytes/immunology ; CD4-Positive T-Lymphocytes/metabolism ; Case-Control Studies ; Female ; Genetic Variation ; HLA-DQ beta-Chains/genetics ; HLA-DQ beta-Chains/immunology ; Humans ; Immunologic Factors/therapeutic use ; Interferon Regulatory Factors/genetics ; Interferon Regulatory Factors/metabolism ; Interferon beta-1a/therapeutic use ; Male ; Middle Aged ; Multiple Sclerosis, Relapsing-Remitting/blood ; Multiple Sclerosis, Relapsing-Remitting/drug therapy ; Multiple Sclerosis, Relapsing-Remitting/genetics ; Multiple Sclerosis, Relapsing-Remitting/immunology ; Phenotype ; Treatment Failure ; Young Adult
Chemical Substances	HLA-DQ beta-Chains ; HLA-DQB1 antigen ; Immunologic Factors ; Interferon Regulatory Factors ; Interferon beta-1a (XRO4566Q4R)
Language	English
Publishing date	2021-05-25
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2021.628375
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article: CD28-mediated co-stimulation: a quantitative support for TCR signalling.

Acuto, Oreste / Michel, Frédérique

Nature reviews. Immunology

2003 Volume 3, Issue 12, Page(s) 939–951

MeSH term(s)	Adaptor Proteins, Signal Transducing ; Animals ; CD28 Antigens/immunology ; Carrier Proteins/immunology ; Cell Cycle/immunology ; Humans ; Lymphocyte Activation/immunology ; Membrane Proteins/immunology ; Mice ; Phosphatidylinositol 3-Kinases/immunology ; Phosphoproteins/immunology ; Signal Transduction/immunology ; T-Lymphocytes/immunology
Chemical Substances	Adaptor Proteins, Signal Transducing ; CD28 Antigens ; Carrier Proteins ; LAT protein, human ; Lat protein, mouse ; Membrane Proteins ; Phosphoproteins ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-)
Language	English
Publishing date	2003-12
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2062776-2
ISSN	1474-1741 ; 1474-1733
ISSN (online)	1474-1741
ISSN	1474-1733
DOI	10.1038/nri1248
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 5565: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 34: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article: Tailoring T-cell receptor signals by proximal negative feedback mechanisms.

Acuto, Oreste / Di Bartolo, Vincenzo / Michel, Frédérique

Nature reviews. Immunology

2008 Volume 8, Issue 9, Page(s) 699–712

Abstract: The T-cell receptor (TCR) signalling machinery is central in determining the response of a T cell (establishing immunity or tolerance) following exposure to antigen. This process is made difficult by the narrow margin of self and non-self discrimination, ...

Abstract	The T-cell receptor (TCR) signalling machinery is central in determining the response of a T cell (establishing immunity or tolerance) following exposure to antigen. This process is made difficult by the narrow margin of self and non-self discrimination, and by the complexity of the genetic programmes that are induced for each outcome. Recent studies have identified novel negative feedback mechanisms that are rapidly induced by TCR engagement and that have key roles in the regulation of signal triggering and propagation. In vitro and in vivo data suggest that they are important in determining ligand discrimination by the TCR and in regulating signal output in response to antigen.
MeSH term(s)	Adaptor Proteins, Signal Transducing/immunology ; Animals ; Feedback, Physiological ; Models, Immunological ; Phosphoric Monoester Hydrolases/metabolism ; Receptors, Antigen, T-Cell/immunology ; Signal Transduction/immunology
Chemical Substances	Adaptor Proteins, Signal Transducing ; Receptors, Antigen, T-Cell ; Phosphoric Monoester Hydrolases (EC 3.1.3.2)
Language	English
Publishing date	2008-09
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2062776-2
ISSN	1474-1741 ; 1474-1733
ISSN (online)	1474-1741
ISSN	1474-1733
DOI	10.1038/nri2397
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 5565: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 34: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Type I interferon potentiates T-cell receptor mediated induction of IL-10-producing CD4⁺ T cells.

Corre, Béatrice / Perrier, Julie / El Khouri, Margueritte / Cerboni, Silvia / Pellegrini, Sandra / Michel, Frédérique

European journal of immunology

2013 Volume 43, Issue 10, Page(s) 2730–2740

Abstract: Type I interferons (IFNs) have the dual ability to promote the development of the immune response and exert an anti-inflammatory activity. We analyzed the integrated effect of IFN-α, TCR signal strength, and CD28 costimulation on human CD4⁺ T-cell ... ...

Abstract	Type I interferons (IFNs) have the dual ability to promote the development of the immune response and exert an anti-inflammatory activity. We analyzed the integrated effect of IFN-α, TCR signal strength, and CD28 costimulation on human CD4⁺ T-cell differentiation into cell subsets producing the anti- and proinflammatory cytokines IL-10 and IFN-γ. We show that IFN-α boosted TCR-induced IL-10 expression in activated peripheral CD45RA⁺CD4⁺ T cells and in whole blood cultures. The functional cooperation between TCR and IFN-α efficiently occurred at low engagement of receptors. Moreover, IFN-α rapidly cooperated with anti-CD3 stimulation alone. IFN-α, but not IL-10, drove the early development of type I regulatory T cells that were mostly IL-10⁺ Foxp3⁻ IFN-γ⁻ and favored IL-10 expression in a fraction of Foxp3⁺ T cells. Our data support a model in which IFN-α costimulates TCR toward the production of IL-10 whose level can be amplified via an autocrine feedback loop.
MeSH term(s)	CD28 Antigens/immunology ; Cell Differentiation/immunology ; Cells, Cultured ; Feedback, Physiological ; Forkhead Transcription Factors/metabolism ; Humans ; Inflammation Mediators/metabolism ; Interferon-alpha/immunology ; Interferon-gamma/metabolism ; Interleukin-10/metabolism ; Leukocyte Common Antigens/metabolism ; Lymphocyte Activation ; Protein Binding ; Receptor Cross-Talk/immunology ; Receptors, Antigen, T-Cell/immunology ; Receptors, Antigen, T-Cell/metabolism ; Signal Transduction/immunology ; T-Lymphocyte Subsets/immunology ; T-Lymphocytes, Regulatory/immunology
Chemical Substances	CD28 Antigens ; FOXP3 protein, human ; Forkhead Transcription Factors ; Inflammation Mediators ; Interferon-alpha ; Receptors, Antigen, T-Cell ; Interleukin-10 (130068-27-8) ; Interferon-gamma (82115-62-6) ; Leukocyte Common Antigens (EC 3.1.3.48)
Language	English
Publishing date	2013-10
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	120108-6
ISSN	1521-4141 ; 0014-2980
ISSN (online)	1521-4141
ISSN	0014-2980
DOI	10.1002/eji.201242977
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 489: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 85: Show issues

Order via subito

Details ▾

To top

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito