Abstract
Severe asthma represents a distinct, poorly-understood phenotype of asthma that has higher morbidity, mortality and a disproportionate need for health care support. Studies have indicated the presence of a specific inflammatory response in severe asthmatics, including the paucity of expression of classical Th-2 type cytokines. Following antigenic stimulation, naive CD4+ T cells proliferate and differentiate into various effector subsets such as Th-1 and Th-2 cells. A third subset of CD4+ T cells has recently been identified and designated as Th-17 cells, which produce IL-17A and F, IL-6, and TNF-α. In severe asthma, there may be a predominant Th-17 phenotype. These cells may promote the release of neutrophil chemotactic factors and induce the expression of GR-β, which is responsible for corticosteroid hyporesponsiveness in immune and structural cells. If the role of Th-17 cytokines is confirmed, it might provide a new option in controlling this refractory subtype of asthma.
Original language | English |
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Pages (from-to) | 41-44 |
Number of pages | 4 |
Journal | Journal of Asthma |
Volume | 45 |
Issue number | SUPPL. 1 |
DOIs | |
Publication status | Published - 2008 |
Keywords
- Cytokines
- Inflammation
- Neutrophil
- Phenotype
- Severe asthma
- Th-17 cells
ASJC Scopus subject areas
- Pediatrics, Perinatology, and Child Health
- Immunology and Allergy
- Pulmonary and Respiratory Medicine