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机构地区:[1]广西医科大学第一附属医院呼吸内科,南宁530021
出 处:《国际免疫学杂志》2010年第5期354-357,共4页International Journal of Immunology
基 金:国家自然科学基金资助项目(30860106);广西科学基金(桂科青0991029)
摘 要:由于长期吸烟的刺激,活化的辅助性T细胞17(Th17)能浸润到肺组织并参与肺泡壁的破坏及肺气肿的形成.Th17细胞在IL-23的作用下,分泌IL-17、IL-21、IL-22等多种细胞因子,其中IL-17可以促进气道中性粒细胞的募集和激活,IL-21在维持、增强Th17细胞的数量及功能的同时,能增加CD8+细胞的数量及其细胞毒活性,在吸烟诱导的慢性阻塞性疾病(COPD)肺部连续炎症中发挥持续放大效应.在不同的炎症环境中,Th17细胞及其分泌的细胞因子与Th1细胞、调节性T细胞(Treg)以及多种参与固有免疫应答的细胞间相互作用和调节,共同参与COPD的发病,并构成了固有免疫与适应性免疫之间的桥梁.Stimulated by long-term smoking, activated secondary T helper 17 cells(Th17) can infiltrate into lung tissue and participate in the destruction of alveolar walls and the formation of emphysema. Under the effect of IL-23, Th17 cells can secrete IL-17, IL-21, IL-22 and other cytokines. IL-17 can promote the recruitment and activation of neutrophils,and IL-21 can maintain and enhance the number and function of Th17 cells and increase the number of CD8 + cells and their cytotoxic activity at the same time. All of the cytokies secreted by activated Th17 play a sustained amplification role in the chronic obstructive pulmonory disease (COPD) continuous lung inflammation. In different inflammatory conditions, Th17 cells and their secreted cytokines interact with and regulate Th1 ,regulatory T(Treg) cells and a variety of natural immune response cells.Consequently,Th17 participate in the pathogenesis of COPD by building the bridge between innate immunity and acquired immunity.
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