Tetraspanin CD53 Promotes Inflammation but Restrains Mucus Production in a Mouse Model of Allergic Airway Inflammation

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985823%3A_____%2F25%3A00604926" target="_blank" >RIV/67985823:_____/25:00604926 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/68378050:_____/25:00604926

Výsledek na webu

<a href="https://onlinelibrary.wiley.com/doi/10.1111/all.16426" target="_blank" >https://onlinelibrary.wiley.com/doi/10.1111/all.16426</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1111/all.16426" target="_blank" >10.1111/all.16426</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Tetraspanin CD53 Promotes Inflammation but Restrains Mucus Production in a Mouse Model of Allergic Airway Inflammation

Popis výsledku v původním jazyce

CD53 is a pan-leukocyte tetraspanin implicated in asthma risk through genome-wide association studies. This study investigates the role of CD53 in IgE-antigen-mediated activation of mast cells and a preclinical mouse model of ovalbumin-induced allergic asthma. Bone marrow-derived mast cells from Cd53-deficient (Cd53-/-) and wild-type (WT) mice were used to examine antigen-IgE-induced mast cell responses. CD53 deficiency did not affect mast cell degranulation but significantly enhanced IgE-antigen-dependent production of pro-inflammatory cytokines, including TNF-α, IL-6, and IL-13. Mechanistically, CD53 deficiency prolonged phosphorylation of c-Jun N-terminal kinase (JNK) and increased nuclear factor-κB (NF-κB) activation. In vivo, using a type 2 allergic asthma model, the absence of CD53 resulted in reduced pulmonary leukocyte infiltration and IgE production but increased mucin gene expression. These changes correlated with impaired lung function measures, including increased tissue damping and elastance. These findings suggest that CD53 plays complex and multifaceted roles in asthma, promoting inflammatory leukocyte recruitment and IgE production while negatively regulating mucus production. In mast cells, CD53 appears to limit IgE-antigen-dependent cytokine production via signaling pathways involving NF-κB and JNK

Název v anglickém jazyce

Tetraspanin CD53 Promotes Inflammation but Restrains Mucus Production in a Mouse Model of Allergic Airway Inflammation

Popis výsledku anglicky

CD53 is a pan-leukocyte tetraspanin implicated in asthma risk through genome-wide association studies. This study investigates the role of CD53 in IgE-antigen-mediated activation of mast cells and a preclinical mouse model of ovalbumin-induced allergic asthma. Bone marrow-derived mast cells from Cd53-deficient (Cd53-/-) and wild-type (WT) mice were used to examine antigen-IgE-induced mast cell responses. CD53 deficiency did not affect mast cell degranulation but significantly enhanced IgE-antigen-dependent production of pro-inflammatory cytokines, including TNF-α, IL-6, and IL-13. Mechanistically, CD53 deficiency prolonged phosphorylation of c-Jun N-terminal kinase (JNK) and increased nuclear factor-κB (NF-κB) activation. In vivo, using a type 2 allergic asthma model, the absence of CD53 resulted in reduced pulmonary leukocyte infiltration and IgE production but increased mucin gene expression. These changes correlated with impaired lung function measures, including increased tissue damping and elastance. These findings suggest that CD53 plays complex and multifaceted roles in asthma, promoting inflammatory leukocyte recruitment and IgE production while negatively regulating mucus production. In mast cells, CD53 appears to limit IgE-antigen-dependent cytokine production via signaling pathways involving NF-κB and JNK

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30102 - Immunology

Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2025

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Allergy

ISSN

0105-4538

e-ISSN

1398-9995

Svazek periodika

80

Číslo periodika v rámci svazku

4

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

5

Strana od-do

1127-1131

Kód UT WoS článku

001375442900001

EID výsledku v databázi Scopus

2-s2.0-85211155709