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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…mehr

Produktbeschreibung
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-alpha. 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-beta, 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.
Autorenporträt
Licenciada en Ciencias (especialidad de Fisiología) y Máster en Ciencias (Patología) por la Universidad McGill. Completé mi licenciatura en medicina en la Universidad Nacional de Irlanda, Galway con un título MBBChBAO. Tengo un gran interés en la investigación clínica, el desarrollo y la enseñanza. Actualmente cursando una especialización quirúrgica en Irlanda.