Businaro R, Digregorio M, Riganò R, Profumo E, Buttari B, Leone S, Salvati B, Capoano R, D'Amati G, Fumagalli L
Department of Cardiovascular Sciences, University of Rome La Sapienza, Rome, Italy.
Ital J Anat Embryol. 2005;110(2 Suppl 1):109-15.
Atherosclerosis is considered a chronic inflammatory process, prompted by lipid accumulation and propagated by cell-mediated mechanisms. The present work was undertaken to clarify this process by characterizing cellular components of inflammatory infiltrate localized within atheroma. Cryostat sections of atherosclerotic lesions obtained from human carotid endarterectomy were analysed immunohistochemically by using monoclonal and polyclonal antibody directed against T cell subpopulations (CD3, CD4, CD8), B cells (CD20), plasma cells (CD138), macrophages (CD14), mast cells (anti-tryptase). Our results assess that T cells are the predominant cell type among plaque infiltrating inflammatory cells. B cells were detected near the lipid core of atheroma and clusters of plasma cells were observed within cellular infiltrates in most plaques. Numerous tryptase positive mast cells were noticed in many areas of complicated lesions. Our results indicate the presence of many inflammatory cells within type V and VI atherosclerotic plaques, suggesting the involvement of those cells in plaque progression. In fact it was previously shown that stability of atherosclerotic lesions is influenced by mast cell-released matrix metalloproteinases which induce plaque rupture and by cytokines and chemokines which increase local inflammatory response and are produced by lymphocytes and macrophages.
动脉粥样硬化被认为是一种慢性炎症过程，由脂质积累引发，并通过细胞介导机制传播。本研究旨在通过对动脉粥样硬化斑块内炎症浸润的细胞成分进行表征来阐明这一过程。使用针对T细胞亚群（CD3、CD4、CD8）、B细胞（CD20）、浆细胞（CD138）、巨噬细胞（CD14）、肥大细胞（抗胰蛋白酶）的单克隆和多克隆抗体，对从人类颈动脉内膜切除术获得的动脉粥样硬化病变的冰冻切片进行免疫组织化学分析。我们的结果评估显示，T细胞是斑块浸润性炎症细胞中占主导地位的细胞类型。在动脉粥样硬化斑块的脂质核心附近检测到B细胞，并且在大多数斑块的细胞浸润内观察到浆细胞簇。在复杂病变的许多区域发现了大量的胰蛋白酶阳性肥大细胞。我们的结果表明，V型和VI型动脉粥样硬化斑块内存在许多炎症细胞，提示这些细胞参与了斑块进展。事实上，先前的研究表明，动脉粥样硬化病变的稳定性受到肥大细胞释放的诱导斑块破裂的基质金属蛋白酶以及由淋巴细胞和巨噬细胞产生的增加局部炎症反应的细胞因子和趋化因子的影响。
