Nicod Laurent P
Clinic and Policlinic of Pneumology, Inselspital, CH 3010 Bern, Switzerland.
Proc Am Thorac Soc. 2006 Jul;3(5):444-9. doi: 10.1513/pats.200601-007AW.
Post-transplant bronchiolitis obliterans, also called bronchiolitis obliterans syndrome, affects up to 50-60% of patients who survive 5 yr after surgery according to its clinical definition, which is based on the degree of obstructive airway disease. Alloimmune-independent and -dependent mechanisms produce injuries and inflammation of epithelial cells and subepithelial structures, leading to aberrant tissue repair. The triggering of innate immunity by various infections or chemical injuries after, for example, gastroesophageal reflux, may lead to the release of danger signals that are able to activate dendritic cells, a crucial link with adaptive immunity. Inflammation can also increase the expression and display of major histocompatibility alloantigens and thus favor the initiation of rejection episodes. These phenomena may be limited in time and location or may be protracted. Reducing the risk of alloimmune-independent factors may be as important as treating acute episodes of lung rejection. Excessive immunosuppression may be deleterious by increasing the risk of infection, thereby triggering innate and adaptive immunity. New potential therapeutic targets are emerging from the research performed on leukotriene receptors, chemokine receptors, and growth factors. Neutralizing these molecules reduces the initial mononuclear and polynuclear infiltrates or the subsequent fibroproliferative process and the neovascular changes, feeding this process.
移植后闭塞性细支气管炎，也称为闭塞性细支气管炎综合征，根据其基于气道阻塞性疾病程度的临床定义，影响高达50%至60%术后存活5年的患者。同种免疫非依赖性和依赖性机制会导致上皮细胞和上皮下结构的损伤与炎症，进而引发异常的组织修复。例如，胃食管反流后各种感染或化学损伤引发的固有免疫，可能导致能够激活树突状细胞的危险信号释放，这是与适应性免疫的关键联系。炎症还可增加主要组织相容性同种抗原的表达和展示，从而有利于排斥反应的启动。这些现象可能在时间和位置上受到限制，也可能持续存在。降低同种免疫非依赖性因素的风险可能与治疗肺排斥急性发作同样重要。过度免疫抑制可能会因增加感染风险而有害，从而引发固有免疫和适应性免疫。对白三烯受体、趋化因子受体和生长因子的研究正在涌现新的潜在治疗靶点。中和这些分子可减少最初的单核和多核浸润，或减少随后的纤维增生过程和新生血管变化，为这一过程提供支持。
