Hart Simon P, Alexander Karen M, Dransfield Ian
Medical Research Council Center for Inflammation Research, University of Edinburgh Medical School, Edinburgh, United Kingdom.
J Immunol. 2004 Feb 1;172(3):1882-7. doi: 10.4049/jimmunol.172.3.1882.
Many human inflammatory diseases are associated with tissue deposition of immune complexes and influx of neutrophils. We show that immune complexes bind preferentially to apoptotic neutrophils via FcgammaRIIA (CD32) and that increased binding is associated with clustering of immune complexes on the plasma membrane of the apoptotic cell. Phagocytosis of immune complex-opsonized apoptotic neutrophils by human macrophages was substantially enhanced (4.4-fold increase compared with control apoptotic neutrophils) and stimulated macrophages to release the proinflammatory cytokines TNF-alpha and IL-6. Immune complexes may perturb the normal pathways for clearance of apoptotic neutrophils by augmenting their clearance at the price of proinflammatory cytokine release. This represents a novel mechanism by which immune complexes may modulate the resolution of inflammation.
许多人类炎症性疾病与免疫复合物的组织沉积和中性粒细胞的流入有关。我们发现免疫复合物通过FcγRIIA（CD32）优先结合凋亡的中性粒细胞，并且结合增加与免疫复合物在凋亡细胞质膜上的聚集有关。人巨噬细胞对免疫复合物调理的凋亡中性粒细胞的吞噬作用显著增强（与对照凋亡中性粒细胞相比增加了4.4倍），并刺激巨噬细胞释放促炎细胞因子TNF-α和IL-6。免疫复合物可能通过以促炎细胞因子释放为代价增强凋亡中性粒细胞的清除来扰乱其正常清除途径。这代表了免疫复合物可能调节炎症消退的一种新机制。
