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小鼠肿瘤浸润淋巴细胞长期培养中非细胞溶解性NK1.1 + T细胞的出现：转化生长因子-β的可能作用

The emergence of non-cytolytic NK1.1+ T cells in the long-term culture of murine tumour-infiltrating lymphocytes: a possible role of transforming growth factor-beta.

作者信息

Tamada K, Harada M, Ito O, Takenoyama M, Mori T, Matsuzaki G, Nomoto K

机构信息

Department of Immunology, Kyushu University, Fukuoka, Japan.

出版信息

Immunology. 1996 Dec;89(4):627-35. doi: 10.1046/j.1365-2567.1996.d01-771.x.

DOI:10.1046/j.1365-2567.1996.d01-771.x
PMID:9014832
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1456569/
Abstract

The mechanism by which murine tumour-infiltrating lymphocytes (TIL) decreased their anti-tumour activity during an in vitro culture with interleukin-2 (IL-2) was investigated. A phenotype analysis revealed that the TIL cultured for 7 days (TIL-d7) were exclusively NKI.1- CD4- CD8+ CD3+ cells and that this population was replaced by natural killer (NK)1.1+ CD4- CD8 CD3+ cells by day 27 (TIL-d27) during the culture of TIL. The TIL-d7 cells showed a cytolytic activity against B16 melanoma, whereas the TIL-d27 cells had lost this activity, suggesting that the decrease in the anti tumour effect of TIL during the culture with IL-2 was due to their populational change. Analysis on the characteristics of the TIL-d27 cells revealed that they expressed skewed T-cell receptor (TCR) V beta 5 and increased mRNA expression of V alpha 14. In addition, they expressed transforming growth factor beta (TGF-beta) mRNA. Interestingly, TGF-beta augmented the proliferation of TIL-d27 cells under the presence of IL-2, but suppressed that of TIL-d7 cells. Moreover, the proliferation of TIL-d27 cells was suppressed by anti-TGF-beta monoclonal antibody. Collectively, these results suggest that, in contrast to its suppressive effect on anti-tumour effector T cells. TGF-beta could be an autocrine growth factor for NKL1.1+ T cells and thereby induce non-cytolytic NK1.1+ T cells in the long-term culture of TIL.

摘要

研究了小鼠肿瘤浸润淋巴细胞（TIL）在白细胞介素-2（IL-2）体外培养过程中其抗肿瘤活性降低的机制。表型分析显示，培养7天的TIL（TIL-d7）仅为NKI.1-CD4-CD8+CD3+细胞，并且在TIL培养过程中，到第27天（TIL-d27）该群体被自然杀伤（NK）1.1+CD4-CD8-CD3+细胞取代。TIL-d7细胞对B16黑色素瘤具有细胞溶解活性，而TIL-d27细胞则失去了这种活性，这表明在IL-2培养过程中TIL抗肿瘤作用的降低是由于其群体变化。对TIL-d27细胞特征的分析表明，它们表达偏斜的T细胞受体（TCR）Vβ5且Vα14的mRNA表达增加。此外，它们表达转化生长因子β（TGF-β）mRNA。有趣的是，在IL-2存在的情况下，TGF-β增强了TIL-d27细胞的增殖，但抑制了TIL-d7细胞的增殖。此外，抗TGF-β单克隆抗体抑制了TIL-d27细胞的增殖。总体而言，这些结果表明，与它对抗肿瘤效应T细胞的抑制作用相反，TGF-β可能是NK1.1+T细胞的自分泌生长因子，从而在TIL的长期培养中诱导非细胞溶解的NK1.1+T细胞。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c65/1456569/ee8e32ea15ab/immunology00030-0160-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c65/1456569/35f9dff70ea3/immunology00030-0159-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c65/1456569/ee8e32ea15ab/immunology00030-0160-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c65/1456569/35f9dff70ea3/immunology00030-0159-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c65/1456569/ee8e32ea15ab/immunology00030-0160-a.jpg

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本文引用的文献

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CD8 T细胞转变为产生TH2细胞因子并辅助B细胞的非细胞溶解性CD8-CD4-细胞。
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NK1.1+ CD4+ CD8- thymocytes with specific lymphokine secretion.具有特异性淋巴因子分泌功能的NK1.1⁺ CD4⁺ CD8⁻ 胸腺细胞。
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