Abstract | PURPOSE OF REVIEW: RECENT FINDINGS: Accumulating data indicate that basophils contribute to endothelium-related IL-4-dependent inflammation. There is also a dendritic cell-related alternative for the induction of Th2 cells via Notch signalling. GATA3 deoxyribozyme improves asthma that is not clearly related to T-cells. The innate immune response in allergy is linked to mast cells, basophils, and the innate lymphoid cell type 2 (ILC2). ILC2s respond to IL-25, IL-33, thymic stromal lymphopoietin, and leukotrienes by producing IL-4, IL-5, and IL-13. In addition to all this inflammatory-cell-driven asthma, increasing evidence has emerged relating to smooth muscle cell activation, the endothelial and epithelial barrier functions, and improvements in the barrier function. The elevation of intracellular cyclic adenosine monophosphate because of the use of phosphodiesterase inhibitors adds to the prevention of epithelial-endothelial leakage, supports airway smooth muscle relaxation, and is immunosuppressive. CONCLUSION AND SUMMARY:
IL-4 is the predominant Th2 cell cytokine. Many more cells, including eosinophils, basophils, mast cells, and ILC2, contribute to the production of IL-4 in the airways. Epithelial cells and endothelial cells lose barrier function in the context of allergic airway inflammation, and this could be at least partially remedied by increasing the intracellular cyclic adenosine monophosphate levels through phosphodiesterase inhibition.
|
Authors | Alex KleinJan |
Journal | Current opinion in pulmonary medicine
(Curr Opin Pulm Med)
Vol. 22
Issue 1
Pg. 46-52
(Jan 2016)
ISSN: 1531-6971 [Electronic] United States |
PMID | 26574718
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
|
Chemical References |
|
Topics |
- Animals
- Asthma
(immunology)
- Cytokines
(immunology)
- Epithelial Cells
(immunology)
- Humans
- Immunity, Innate
(immunology)
- Inflammation
(immunology)
- Th2 Cells
(immunology)
|