Matches in SemOpenAlex for { <https://semopenalex.org/work/W4385685619> ?p ?o ?g. }
Showing items 1 to 77 of
77
with 100 items per page.
- W4385685619 endingPage "67.08" @default.
- W4385685619 startingPage "67.08" @default.
- W4385685619 abstract "Abstract Group 3 innate lymphoid cells (ILC3s) are involved in air pollution- and bacterial infection-associated neutrophilic asthma. Studies showed that asthmatic patients have higher stem cell factor (SCF) expression in airway and sera. Of note, ILC3s express SCF receptor, c-Kit, suggesting a potential role of SCF/c-Kit signaling in ILC3 functions and neutrophilic asthma. In this study, we aimed to determine whether SCF/c-Kit signaling could modulate ILC3 functions and neutrophilic asthma. Wild-type (WT) and c-Kit deficient mice (Kit w-sh) were intranasally treated with IL-1β/IL-23 or particulate matter (PM) 2.5 to induce neutrophilic asthma. While IL-1β/IL-23 or PM2.5 caused increases in neutrophil infiltration to bronchoalveolar lavage fluid (BALF) and airway hyperreactivity (AHR) in WT mice, Kit w-shmice had decreased infiltration of neutrophils and ameliorated AHR. Concomitantly, flow cytometry results showed a decreased number of IL-17+ ILC3 in the lung of Kit w-shmice compared to WT mice, which may be due to the reduced proliferation of c-Kit-deficient ILC3. In addition, we showed SCF enhanced IL-17 secretion from ILC3s in vitro. Based on re-analysis of published mouse whole lung cells scRNAseq data, we hypothesized fibroblasts are the source of SCF. Indeed, mice with SCF knockout in fibroblast exhibited decreased neutrophil infiltration and reduced IL-17+ ILC3 number in response to IL-1β/IL-23. Finally, administration of imatinib, a FDA-approved drug targeting c-Kit signaling, ameliorated AHR and ILC3 activation in the mouse neutrophilic asthma model. Taken together, our data suggested that inhibition of ILC3 activation by targeting c-Kit signaling may provide a potential therapeutic management for neutrophilic asthma." @default.
- W4385685619 created "2023-08-10" @default.
- W4385685619 creator A5008570342 @default.
- W4385685619 creator A5066249910 @default.
- W4385685619 creator A5066430136 @default.
- W4385685619 date "2023-05-01" @default.
- W4385685619 modified "2023-09-27" @default.
- W4385685619 title "c-Kit signaling modulated group 3 innate lymphoid cell functions in mouse neutrophilic asthma model" @default.
- W4385685619 doi "https://doi.org/10.4049/jimmunol.210.supp.67.08" @default.
- W4385685619 hasPublicationYear "2023" @default.
- W4385685619 type Work @default.
- W4385685619 citedByCount "0" @default.
- W4385685619 crossrefType "journal-article" @default.
- W4385685619 hasAuthorship W4385685619A5008570342 @default.
- W4385685619 hasAuthorship W4385685619A5066249910 @default.
- W4385685619 hasAuthorship W4385685619A5066430136 @default.
- W4385685619 hasBestOaLocation W43856856191 @default.
- W4385685619 hasConcept C109159458 @default.
- W4385685619 hasConcept C121332964 @default.
- W4385685619 hasConcept C126322002 @default.
- W4385685619 hasConcept C153400128 @default.
- W4385685619 hasConcept C2022786 @default.
- W4385685619 hasConcept C203014093 @default.
- W4385685619 hasConcept C2776042228 @default.
- W4385685619 hasConcept C2777714996 @default.
- W4385685619 hasConcept C2777961210 @default.
- W4385685619 hasConcept C2779341262 @default.
- W4385685619 hasConcept C2779727006 @default.
- W4385685619 hasConcept C28328180 @default.
- W4385685619 hasConcept C47742525 @default.
- W4385685619 hasConcept C553184892 @default.
- W4385685619 hasConcept C71924100 @default.
- W4385685619 hasConcept C74737994 @default.
- W4385685619 hasConcept C86803240 @default.
- W4385685619 hasConcept C8891405 @default.
- W4385685619 hasConcept C95444343 @default.
- W4385685619 hasConcept C97355855 @default.
- W4385685619 hasConceptScore W4385685619C109159458 @default.
- W4385685619 hasConceptScore W4385685619C121332964 @default.
- W4385685619 hasConceptScore W4385685619C126322002 @default.
- W4385685619 hasConceptScore W4385685619C153400128 @default.
- W4385685619 hasConceptScore W4385685619C2022786 @default.
- W4385685619 hasConceptScore W4385685619C203014093 @default.
- W4385685619 hasConceptScore W4385685619C2776042228 @default.
- W4385685619 hasConceptScore W4385685619C2777714996 @default.
- W4385685619 hasConceptScore W4385685619C2777961210 @default.
- W4385685619 hasConceptScore W4385685619C2779341262 @default.
- W4385685619 hasConceptScore W4385685619C2779727006 @default.
- W4385685619 hasConceptScore W4385685619C28328180 @default.
- W4385685619 hasConceptScore W4385685619C47742525 @default.
- W4385685619 hasConceptScore W4385685619C553184892 @default.
- W4385685619 hasConceptScore W4385685619C71924100 @default.
- W4385685619 hasConceptScore W4385685619C74737994 @default.
- W4385685619 hasConceptScore W4385685619C86803240 @default.
- W4385685619 hasConceptScore W4385685619C8891405 @default.
- W4385685619 hasConceptScore W4385685619C95444343 @default.
- W4385685619 hasConceptScore W4385685619C97355855 @default.
- W4385685619 hasIssue "1_Supplement" @default.
- W4385685619 hasLocation W43856856191 @default.
- W4385685619 hasOpenAccess W4385685619 @default.
- W4385685619 hasPrimaryLocation W43856856191 @default.
- W4385685619 hasRelatedWork W1995866594 @default.
- W4385685619 hasRelatedWork W2324953218 @default.
- W4385685619 hasRelatedWork W2415138818 @default.
- W4385685619 hasRelatedWork W2441567832 @default.
- W4385685619 hasRelatedWork W3164497571 @default.
- W4385685619 hasRelatedWork W4220843437 @default.
- W4385685619 hasRelatedWork W4238678312 @default.
- W4385685619 hasRelatedWork W4322724676 @default.
- W4385685619 hasRelatedWork W4323656676 @default.
- W4385685619 hasRelatedWork W4385685619 @default.
- W4385685619 hasVolume "210" @default.
- W4385685619 isParatext "false" @default.
- W4385685619 isRetracted "false" @default.
- W4385685619 workType "article" @default.