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穿孔素在浸润至人结直肠癌的淋巴细胞中的表达。

Perforin expression in lymphocytes infiltrated to human colorectal cancer.

作者信息

Nakanishi H, Monden T, Morimoto H, Kobayashi T, Shimano T, Mori T

机构信息

Department of Surgery II, Osaka University Medical School, Japan.

出版信息

Br J Cancer. 1991 Aug;64(2):239-42. doi: 10.1038/bjc.1991.283.

DOI:10.1038/bjc.1991.283
PMID:1892750
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1977537/
Abstract

Perforin (PFP) is a cytotoxic protein released from killer cells. PFP immunoreactivity in human peripheral blood lymphocytes (PBL) and tumour infiltrating lymphocytes (TIL) was investigated immunocytochemically with the aid of an anti-PFP monoclonal antibody. PFP was detected in the cytoplasm of 10% of PBL. We performed a double staining of PFP+ cells with Leu11b/CD16, Leu2a/CD8, or Leu3a/CD4 and showed that PFP was produced by 9% of CD8+ cells and 18% of CD16+ cells but not by CD4+ cells. In 28 colorectal cancer tissues, PFP immunoreactivity was observed in the lymphocytes infiltrating to the tumour stroma. The PFP+ cells were most numerous in Dukes A and decreased in number according to the progression of tumours. The PFP+ cells in TIL exhibited the same phenotypes as those in PBL but the PFP+ cells were more numerous in CD8+ cells than in CD16+ cells at all stages. This study represents the first evidence that PFP is mainly secreted from CD8+ cells in tumour tissues. It is hypothesised that the decrease in the number of PFP+ cells in accordance with tumour progression may reflect the suppression of the hosts local immunity.

摘要

穿孔素（PFP）是一种从杀伤细胞释放的细胞毒性蛋白。借助抗PFP单克隆抗体，采用免疫细胞化学方法研究了人外周血淋巴细胞（PBL）和肿瘤浸润淋巴细胞（TIL）中的PFP免疫反应性。在10%的PBL细胞质中检测到PFP。我们用Leu11b/CD16、Leu2a/CD8或Leu3a/CD4对PFP+细胞进行双重染色，结果显示9%的CD8+细胞和18%的CD16+细胞产生PFP，而CD4+细胞不产生。在28例结直肠癌组织中，在浸润到肿瘤基质的淋巴细胞中观察到PFP免疫反应性。PFP+细胞在Dukes A期最多，且随着肿瘤进展数量减少。TIL中的PFP+细胞与PBL中的表现出相同的表型，但在所有阶段，CD8+细胞中的PFP+细胞比CD16+细胞中的更多。本研究首次证明PFP主要由肿瘤组织中的CD8+细胞分泌。据推测，随着肿瘤进展PFP+细胞数量的减少可能反映了宿主局部免疫的抑制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f3e/1977537/919f715dd918/brjcancer00072-0043-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f3e/1977537/ea6f864565ec/brjcancer00072-0042-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f3e/1977537/5a7cb6ab6f24/brjcancer00072-0042-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f3e/1977537/23534264055d/brjcancer00072-0042-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f3e/1977537/919f715dd918/brjcancer00072-0043-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f3e/1977537/ea6f864565ec/brjcancer00072-0042-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f3e/1977537/5a7cb6ab6f24/brjcancer00072-0042-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f3e/1977537/23534264055d/brjcancer00072-0042-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f3e/1977537/919f715dd918/brjcancer00072-0043-a.jpg

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本文引用的文献

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