PDF(Pubmed)
Abstract：
Although antibody-mediated lung damage is a major factor in transfusion-related acute lung injury (ALI), autoimmune lung disease (for example, coatomer subunit α [COPA] syndrome), and primary graft dysfunction following lung transplantation, the mechanism by which antigen-antibody complexes activate complement to induce lung damage remains unclear. In this issue of the JCI, Cleary and colleagues utilized several approaches to demonstrate that IgG forms hexamers with MHC class I alloantibodies. This hexamerization served as a key pathophysiological mechanism in alloimmune lung injury models and was mediated through the classical pathway of complement activation. Additionally, the authors provided avenues for exploring therapeutics for this currently hard-to-treat clinical entity that has several etiologies but a potentially focused mechanism.
摘要：
尽管抗体介导的肺损伤是输血相关急性肺损伤（ALI）的主要因素，自身免疫性肺病（例如，coatomer亚基α[COPA]综合征)，和肺移植后的原发性移植物功能障碍，抗原-抗体复合物激活补体诱导肺损伤的机制尚不清楚.在本期JCI中，Cleary及其同事使用了几种方法来证明IgG与MHCI类同种抗体形成六聚体。在同种免疫肺损伤模型中，这种六聚体化是关键的病理生理机制，并通过经典的补体激活途径介导。此外,作者提供了探索这种目前难以治疗的临床实体的治疗方法的途径,该实体有多种病因,但有可能集中在机制上.
