Hogan S P, Foster P S
Cellular Signal Transduction Laboratory, John Curtin School of Medical Research, Australian National University, Canberra, Australia.
Med Res Rev. 1996 Sep;16(5):407-32. doi: 10.1002/(SICI)1098-1128(199609)16:5<407::AID-MED2>3.0.CO;2-Z.
The recruitment of eosinophils to sites of allergic inflammation is a complex process that is primarily regulated by inflammatory cytokines and chemokines. These molecules act in concert to stimulate peripheral eosinophilia, regulate homing of eosinophils to the inflammed organ, and promote eosinophil-vascular endothelium interactions, extravasation, chemotaxis, and localization to the site of the inflammatory stimulus. The essential and specific role of IL-5 in regulating blood and tissue eosinophilia, and the subsequent involvement of this leukocyte in the induction of lung damage and airway dysfunction identifies IL-5 as a primary therapeutic target. Developing strategies to inhibit IL-5 production and action, such as by the delivery of inhibitory cytokines to the lung, which specifically down-regulate CD4+ TH2 cell responses and eosinophilic inflammation, may be more beneficial than the current drugs of choice for preventive treatment and in the relief of acute and chronic asthma and allergic disease.
嗜酸性粒细胞募集至变应性炎症部位是一个复杂的过程，主要由炎性细胞因子和趋化因子调控。这些分子协同作用，刺激外周嗜酸性粒细胞增多，调节嗜酸性粒细胞向炎症器官的归巢，并促进嗜酸性粒细胞与血管内皮的相互作用、渗出、趋化作用以及向炎症刺激部位的定位。白细胞介素-5在调节血液和组织嗜酸性粒细胞增多方面的关键且特异性作用，以及这种白细胞随后参与肺损伤和气道功能障碍的诱导，确定白细胞介素-5为主要治疗靶点。开发抑制白细胞介素-5产生和作用的策略，例如通过向肺递送抑制性细胞因子，特异性下调CD4⁺ TH2细胞反应和嗜酸性粒细胞炎症，可能比目前用于预防性治疗以及缓解急性和慢性哮喘及变应性疾病的首选药物更有益。
