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Stem cell therapy in animal models of allergic airway diseases
Allergy, Asthma & Respiratory Disease ; : 167-173, 2016.
Article Dans Coréen | WPRIM | ID: wpr-108729
ABSTRACT
Allergic airway diseases are characterized by T-helper type 2 (Th2)-skewed eosinophilic inflammation, mucus hypersecretion, and airway hyperresponsiveness. The excessive activation of Th2 cells due to insufficient suppression of regulatory T cells (Tregs) is thought to play a major role in the initiation and development of allergic airway disease. Several studies have shown that stem cells provide a significant reduction in allergic airway inflammation and improve lung function in animal models. The immunomodulatory effects of stem cells in allergic airway disease may be mediated by the up-regulation of Tregs and increases in several soluble factors, such as prostaglandin E2, transforming growth factor-β, interleukin-10, and indoleamine 2, 3-dioxygenase. This review examines the current understanding of the immunomodulatory properties of stem cells and its therapeutic implication in allergic airway disease. Furthermore, we will discuss mechanisms by which stem cells inhibit allergic airway inflammation via immunomodulation from a Th2- to a Th1-biased response.
Sujets)

Texte intégral: Disponible Indice: WPRIM (Pacifique occidental) Sujet Principal: Asthme / Cellules souches / Dinoprostone / Régulation positive / Immunosuppression thérapeutique / Interleukine-10 / Lymphocytes T régulateurs / Lymphocytes auxiliaires Th2 / Modèles animaux / Granulocytes éosinophiles Limites du sujet: Animaux langue: Coréen Texte intégral: Allergy, Asthma & Respiratory Disease Année: 2016 Type: Article

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Texte intégral: Disponible Indice: WPRIM (Pacifique occidental) Sujet Principal: Asthme / Cellules souches / Dinoprostone / Régulation positive / Immunosuppression thérapeutique / Interleukine-10 / Lymphocytes T régulateurs / Lymphocytes auxiliaires Th2 / Modèles animaux / Granulocytes éosinophiles Limites du sujet: Animaux langue: Coréen Texte intégral: Allergy, Asthma & Respiratory Disease Année: 2016 Type: Article