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坏死性淋巴结炎的免疫组织化学研究:一种涉及产生穿孔素和颗粒酶的细胞毒性T细胞的凋亡可能机制。

Immunohistochemical study of necrotizing lymphadenitis: a possible mechanism for apoptosis involving perforin and granzyme-producing cytotoxic T cells.

作者信息

Mori N, Yatabe Y, Asai J, Nagasawa T

机构信息

First Department of Pathology, Nagoya University, School of Medicine, Japan.

出版信息

Pathol Int. 1997 Jan;47(1):31-7. doi: 10.1111/j.1440-1827.1997.tb04432.x.

Abstract

Twelve lymph node specimens with necrotizing lymphadenitis and which had florid necrotic lesions were studied immunohistochemically. The majority of viable lymphoid cells in the necrotic foci were CD8+ lymphocytes and KP1+ or PGM1+ phagocytizing macrophages. The CD8+ T cells were Leu1+, Leu2+, Leu3-, Leu4+, Leu5b+, Leu7-, Leu11b- and Leu19-, indicating a suppressor/cytotoxic T cell phenotype. In addition, the cytoplasm of these cells was immunoreactive for perforin and granzyme B in a granular pattern. With a nick end-labeling technique, fragmented nuclei and some lymphoid cell nuclei were positively stained. These results suggest that the necrosis in necrotizing lymphadenitis is apoptotic necrosis of T cells targeted by CD8+, perforin and granzyme-producing, activated cytotoxic T cells, supporting a viral infection etiology.

摘要

对12例伴有坏死性淋巴结炎且有明显坏死病变的淋巴结标本进行了免疫组织化学研究。坏死灶中大多数存活的淋巴细胞是CD8 +淋巴细胞以及KP1 +或PGM1 +吞噬性巨噬细胞。CD8 + T细胞为Leu1 +、Leu2 +、Leu3 -、Leu4 +、Leu5b +、Leu7 -、Leu11b -和Leu19 -,表明为抑制性/细胞毒性T细胞表型。此外,这些细胞的胞质对穿孔素和颗粒酶B呈颗粒状免疫反应阳性。采用缺口末端标记技术,破碎的细胞核和一些淋巴细胞核呈阳性染色。这些结果提示,坏死性淋巴结炎中的坏死是由产生穿孔素和颗粒酶的活化细胞毒性CD8 + T细胞靶向的T细胞凋亡性坏死,支持病毒感染病因。

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