Kawasaki disease (KD) is a systemic vasculitis of unknown etiology which predominantly affects medium- and small-sized muscular arteries. Histopathologic studies of KD vasculitis lesions have demonstrated characteristic T cell infiltration and an abundance of CD8+ T cells; however, the contribution of cytotoxic lymphocytes to KD vasculitis lesions has not been identified. Here, we histopathologically and immunohistochemically examined infiltrating inflammatory cells, particularly cytotoxic protein-positive cells, such as granzyme B+ cells and TIA-1+ cells, in KD vasculitis lesions. Three autopsy specimens with acute-phase KD were observed and contained 24 vasculitis lesions affecting medium-sized muscular arteries, excluding pulmonary arteries. Infiltrating neutrophils in vasculitis lesions were evaluated by hematoxylin and eosin staining, and monocytes/macrophages and lymphocytes were evaluated by immunohistochemistry. The predominant cells were CD163+ monocytes/macrophages and CD3+ T cells. CD8+ T cells, granzyme B+ cells, and TIA-1+ cells were also observed, but CD56+ natural killer cells were rare. To the best of our knowledge, the current study is the first histopathologic report confirming the infiltration of inflammatory cells with cytotoxic proteins in vasculitis lesions in patients with KD. Cytotoxic T cells may play a role in the development of vasculitis lesions in KD patients.

中文翻译：

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川崎病动脉炎病变浸润性炎症细胞的组织学和免疫组织化学评估

川崎病（KD）是一种病因不明的全身性血管炎，主要累及中小肌肉动脉。KD 血管炎病变的组织病理学研究显示特征性 T 细胞浸润和大量 CD8+ T 细胞；然而，细胞毒性淋巴细胞对 KD 血管炎病变的贡献尚未确定。在这里，我们通过组织病理学和免疫组织化学检查了 KD 血管炎病变中的浸润性炎症细胞，特别是细胞毒性蛋白阳性细胞，如颗粒酶 B+ 细胞和 TIA-1+ 细胞。观察到三个具有急性期 KD 的尸检标本，其中包含 24 个影响中等大小肌肉动脉的血管炎病变，不包括肺动脉。通过苏木精和伊红染色评估血管炎病变中浸润的中性粒细胞，通过免疫组织化学评估单核细胞/巨噬细胞和淋巴细胞。主要细胞是 CD163+ 单核细胞/巨噬细胞和 CD3+ T 细胞。CD8+ T 细胞、颗粒酶 B+ 细胞和 TIA-1+ 细胞也被观察到，但 CD56+ 自然杀伤细胞很少见。据我们所知，目前的研究是第一个组织病理学报告，证实了 KD 患者血管炎病变中炎症细胞浸润的细胞毒性蛋白。细胞毒性 T 细胞可能在 KD 患者血管炎病变的发展中发挥作用。目前的研究是第一个组织病理学报告，证实了 KD 患者的血管炎病变中炎症细胞浸润了细胞毒性蛋白。细胞毒性 T 细胞可能在 KD 患者血管炎病变的发展中发挥作用。目前的研究是第一个组织病理学报告，证实了 KD 患者血管炎病变中炎症细胞浸润有细胞毒性蛋白。细胞毒性 T 细胞可能在 KD 患者血管炎病变的发展中发挥作用。