title: Th-17 cell-related cytokines' potential role in the pathogenesis of severe asthma.
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-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.
authors.affiliation: Meakins-Christie Laboratories, Montreal Chest Institute, McGill University Hospital Centre, Montreal, QC, Canada.
authors.forename: Wisam
authors.initials: W
authors.lastname: Al-Ramli
authors.forename: Mohamed
authors.initials: M
authors.lastname: Al Samri
authors.forename: Qutayba
authors.initials: Q
authors.lastname: Hamid
mesh_terms: D000818:Animals; D001249:Asthma / Q000209:etiology* / Q000276:immunology; D016207:Cytokines / Q000502:physiology*; D006801:Humans; D016130:Immunophenotyping; D053759:Interleukin-23 / Q000502:physiology; D058504:Th17 Cells / Q000276:immunology*
chemical_list: D016207:Cytokines; D053759:Interleukin-23