Neutrophils in STAT1 Gain-Of-Function Have a Pro-inflammatory Signature Which Is Not Rescued by JAK Inhibition
- Standort
-
Deutsche Nationalbibliothek Frankfurt am Main
- Umfang
-
1 Online-Ressource.
- Sprache
-
Englisch
- Erschienen in
-
Neutrophils in STAT1 Gain-Of-Function Have a Pro-inflammatory Signature Which Is Not Rescued by JAK Inhibition ; volume:43 ; number:7 ; day:26 ; month:6 ; year:2023 ; pages:1640-1659 ; date:10.2023
Journal of clinical immunology ; 43, Heft 7 (26.6.2023), 1640-1659, 10.2023
- Urheber
-
Parackova, Zuzana
Vrabcova, Petra
Zentsova, Irena
Sediva, Anna
Bloomfield, Marketa
- Beteiligte Personen und Organisationen
-
SpringerLink (Online service)
- DOI
-
10.1007/s10875-023-01528-1
- URN
-
urn:nbn:de:101:1-2023112714051864608204
- Rechteinformation
-
Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Letzte Aktualisierung
-
15.08.2025, 07:20 MESZ
Datenpartner
Dieses Objekt wird bereitgestellt von:
Deutsche Nationalbibliothek. Bei Fragen zum Objekt wenden Sie sich bitte an den Datenpartner.
Deutsche Nationalbibliothek. Bei Fragen zum Objekt wenden Sie sich bitte an den Datenpartner.
Beteiligte
- Parackova, Zuzana
- Vrabcova, Petra
- Zentsova, Irena
- Sediva, Anna
- Bloomfield, Marketa
- SpringerLink (Online service)
Ähnliche Objekte (12)
Heterozygous STAT1 gain-of-function mutations underlie an unexpectedly broad clinical phenotype
Rescued
Rescued!
Rescued!
Gain-of-function human STAT1 mutations impair IL-17 immunity and underlie chronic mucocutaneous candidiasis
Two different STAT1 gain-of-function mutations lead to diverse IFN-γ-mediated gene expression
Three Adult Cases of STAT1 Gain-of-Function with Chronic Mucocutaneous Candidiasis Treated with JAK Inhibitors
Patients with STAT1 Gain-of-function Mutations Display Increased Apoptosis which is Reversed by the JAK Inhibitor Ruxolitinib
Bonding the foe – NETting neutrophils immobilize the pro-inflammatory monosodium urate crystals
The Extended Clinical Phenotype of 26 Patients with Chronic Mucocutaneous Candidiasis due to Gain-of-Function Mutations in STAT1
STAT1 gain-of-function and dominant negative STAT3 mutations impair IL-17 and IL-22 immunity associated with CMC
Inhibition of Pro‐Inflammatory Functions of Human Neutrophils by Constituents of Melodorum fruticosum Leaves
Heterozygous STAT1 gain-of-function mutations underlie an unexpectedly broad clinical phenotype
Rescued
Rescued!
Rescued!
Gain-of-function human STAT1 mutations impair IL-17 immunity and underlie chronic mucocutaneous candidiasis
Two different STAT1 gain-of-function mutations lead to diverse IFN-γ-mediated gene expression
Three Adult Cases of STAT1 Gain-of-Function with Chronic Mucocutaneous Candidiasis Treated with JAK Inhibitors
Patients with STAT1 Gain-of-function Mutations Display Increased Apoptosis which is Reversed by the JAK Inhibitor Ruxolitinib
Bonding the foe – NETting neutrophils immobilize the pro-inflammatory monosodium urate crystals
The Extended Clinical Phenotype of 26 Patients with Chronic Mucocutaneous Candidiasis due to Gain-of-Function Mutations in STAT1
STAT1 gain-of-function and dominant negative STAT3 mutations impair IL-17 and IL-22 immunity associated with CMC
Inhibition of Pro‐Inflammatory Functions of Human Neutrophils by Constituents of Melodorum fruticosum Leaves
Heterozygous STAT1 gain-of-function mutations underlie an unexpectedly broad clinical phenotype
Rescued
Rescued!
Rescued!
Gain-of-function human STAT1 mutations impair IL-17 immunity and underlie chronic mucocutaneous candidiasis
Two different STAT1 gain-of-function mutations lead to diverse IFN-γ-mediated gene expression
Three Adult Cases of STAT1 Gain-of-Function with Chronic Mucocutaneous Candidiasis Treated with JAK Inhibitors
Patients with STAT1 Gain-of-function Mutations Display Increased Apoptosis which is Reversed by the JAK Inhibitor Ruxolitinib
Bonding the foe – NETting neutrophils immobilize the pro-inflammatory monosodium urate crystals
The Extended Clinical Phenotype of 26 Patients with Chronic Mucocutaneous Candidiasis due to Gain-of-Function Mutations in STAT1
STAT1 gain-of-function and dominant negative STAT3 mutations impair IL-17 and IL-22 immunity associated with CMC