Department of Biology, College of Science, Salahaddin University- Erbil, Erbil, Iraq.
Cell Mol Biol (Noisy-le-grand). 2024 Sep 8;70(8):50-56. doi: 10.14715/cmb/2024.70.8.6.
Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) is a deadly pulmonary disease with impaired immunological response that causes significant tissue damage and organ failure. Postmortem examination of the lung is a useful tool for understanding the immunopathogenesis of this virus. Lung autopsy samples from seven dead SARS-CoV-2 patients were obtained and evaluated using hematoxylin and eosin stain to analyze the histopathological changes in those samples, on the other hand, Immunohistochemical (IHC) staining was used for detection of CD21, CD1a, CR1 (CD35), CD68, Myeloperoxidase (MPO), CD15, CD56, CD3, CD20, CD4, and CD8 cells markers. Histopathological examination revealed diffuse alveolar damage with extensive parenchymal architecture distortion, intravascular fibrin clot, deposition of collagen fibers, vascular congestions and blood vessels containing thrombi, pneumocyte type II with inflammatory cell infiltration. The IHC staining for the innate immune cells such as antigen-presenting cells (APCs) including dendritic cells, Macrophages, and neutrophils showed a strong positive staining, while CD56 Natural killer (NK) cells showed negative staining. On the other hand, the specific immune cells including; CD20 B cells, CD3 T cells, and CD4 helper T cells, showed positive staining while CD8 Cytotoxic T cells showed negative staining. The lung autopsy samples from patients with COVID-19 confirmed the presence of APCs through the positive staining of CD21, CD1a, CD35, CD68, MPO, and CD15 expressed the virus recognition, proinflammatory cytokine production, and adaptive immune cells activation through CD3, CD4, and CD20 positive staining and the role of APCs in the severity of pulmonary infection and pathogenesis of SARS-CoV-2 infection however the absence of the CD56 NK and CD8 cytotoxic T explains the worse infection status for the patients.
严重急性呼吸综合征冠状病毒 2 型(SARS-CoV-2)是一种具有免疫功能障碍的致命性肺部疾病,可导致严重的组织损伤和器官衰竭。对肺部进行尸检是了解该病毒免疫发病机制的有用工具。对 7 名死于 SARS-CoV-2 的患者的肺尸检样本进行了获取和评估,使用苏木精和伊红染色分析这些样本的组织病理学变化,另一方面,免疫组织化学(IHC)染色用于检测 CD21、CD1a、CR1(CD35)、CD68、髓过氧化物酶(MPO)、CD15、CD56、CD3、CD20、CD4 和 CD8 细胞标志物。组织病理学检查显示弥漫性肺泡损伤,广泛的实质结构扭曲,血管内纤维蛋白凝块,胶原纤维沉积,血管充血和含血栓的血管,Ⅱ型肺泡细胞伴有炎症细胞浸润。天然免疫细胞(如抗原呈递细胞(APC))的 IHC 染色,包括树突状细胞、巨噬细胞和中性粒细胞,呈强阳性染色,而 CD56 自然杀伤(NK)细胞呈阴性染色。另一方面,包括 CD20 B 细胞、CD3 T 细胞和 CD4 辅助性 T 细胞在内的特异性免疫细胞呈阳性染色,而 CD8 细胞毒性 T 细胞呈阴性染色。COVID-19 患者的肺尸检样本通过 CD21、CD1a、CD35、CD68、MPO 和 CD15 的阳性染色证实了 APC 的存在,表达了病毒识别、促炎细胞因子产生和适应性免疫细胞激活,通过 CD3、CD4 和 CD20 的阳性染色,以及 APC 在肺部感染严重程度和 SARS-CoV-2 感染发病机制中的作用,但 CD56 NK 和 CD8 细胞毒性 T 的缺失解释了患者更严重的感染状态。