Inflammation in Asthma Pathogenesis: Role of T Cells, Macrophages,Epithelial Cells and Type 2 Inflammation / Amina Hamed Alobaidi, Abdulghani Mohamed Alsamarai, Mohamed Almoustafa Alsamarai
Asthma is a chronic disease with abnormal inflammatory and immunological responses.The disease initiates by antigens in subjects with genetic susceptibility. However, environmentalfactors play a role in the initiation and exacerbation of asthma attack. Asthma is a T-helper 2(Th2)-cell-mediated disease. Recent studies indicate that asthma is not a single disease entity, but itoccurs with multiple phenotypes and endotypes. The pathophysiological changes in asthma includea series of continuous vicious circles of cellular activation contributing to the induction ofchemokines and cytokines that potentiate inflammation. The heterogeneity of asthma influencesthe treatment response. The asthma pathogenesis is driven by varied sets of cells, such aseosinophils, basophils, neutrophils, macrophages, epithelial cells, and T cells. Macrophages inducea set of mediators that are involved in asthma pathogenesis and include MIF, Prostaglandin, CXCR3L,IL-12, IL-1ß, TSLP, IL-18, IL-33, LTC4, MMP-2, TNF-α, IL-17, IL-10, TGF-ß and IL-27.While, T-cells mediators effect in asthma is induced via TNF-α, IL-17, IL-10, TGF-ß, IL-27, Tim,GM-CSF, IL-2, IL-4, IL-13, INF- γ, and PPAR γ. However, the epithelial cells induced mediatorspotentiate proinflammatory effects, increase the number of Th2 cells, activate dendritic cells, increasethe number of mast cells, and recruit eosinophils, basophils, neutrophils, T-cells, monocytesand dendritic cells. In this review, the role of T cells, macrophages, and epithelial cells is discussed.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2021 |
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| Erschienen: |
2021 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:20 |
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| Enthalten in: |
Anti-inflammatory & anti-allergy agents in medicinal chemistry - 20(2021), 4, Seite 16 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Alobaidi, Amina Hamed [VerfasserIn] |
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| Links: |
FID Access [lizenzpflichtig] |
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| Umfang: |
1 Online-Ressource (16 p) |
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| Förderinstitution / Projekttitel: |
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| 520 | |a Asthma is a chronic disease with abnormal inflammatory and immunological responses.The disease initiates by antigens in subjects with genetic susceptibility. However, environmentalfactors play a role in the initiation and exacerbation of asthma attack. Asthma is a T-helper 2(Th2)-cell-mediated disease. Recent studies indicate that asthma is not a single disease entity, but itoccurs with multiple phenotypes and endotypes. The pathophysiological changes in asthma includea series of continuous vicious circles of cellular activation contributing to the induction ofchemokines and cytokines that potentiate inflammation. The heterogeneity of asthma influencesthe treatment response. The asthma pathogenesis is driven by varied sets of cells, such aseosinophils, basophils, neutrophils, macrophages, epithelial cells, and T cells. Macrophages inducea set of mediators that are involved in asthma pathogenesis and include MIF, Prostaglandin, CXCR3L,IL-12, IL-1ß, TSLP, IL-18, IL-33, LTC4, MMP-2, TNF-α, IL-17, IL-10, TGF-ß and IL-27.While, T-cells mediators effect in asthma is induced via TNF-α, IL-17, IL-10, TGF-ß, IL-27, Tim,GM-CSF, IL-2, IL-4, IL-13, INF- γ, and PPAR γ. However, the epithelial cells induced mediatorspotentiate proinflammatory effects, increase the number of Th2 cells, activate dendritic cells, increasethe number of mast cells, and recruit eosinophils, basophils, neutrophils, T-cells, monocytesand dendritic cells. In this review, the role of T cells, macrophages, and epithelial cells is discussed | ||
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