Al-Ramli Wisam, Al Samri Mohamed, Hamid Qutayba
Meakins-Christie Laboratories, Montreal Chest Institute, McGill University Hospital Centre, Montreal, QC, Canada.
J Asthma. 2008;45 Suppl 1:41-4. doi: 10.1080/02770900802594759.
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.
重度哮喘是一种独特的、尚未被充分理解的哮喘表型，其发病率、死亡率更高，对医疗保健支持的需求也不成比例。研究表明，重度哮喘患者存在特定的炎症反应，包括经典Th-2型细胞因子表达不足。抗原刺激后，初始CD4+ T细胞增殖并分化为各种效应子亚群，如Th-1和Th-2细胞。最近已鉴定出CD4+ T细胞的第三个亚群，并将其命名为Th-17细胞，该细胞可产生IL-17A和F、IL-6以及TNF-α。在重度哮喘中，可能存在主要的Th-17表型。这些细胞可能促进中性粒细胞趋化因子的释放，并诱导GR-β的表达，GR-β负责免疫和结构细胞中的皮质类固醇低反应性。如果Th-17细胞因子的作用得到证实，可能会为控制这种难治性哮喘亚型提供新的选择。
