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淋巴因子激活的杀伤细胞表型的异质性。

Heterogeneity of the lymphokine-activated killer cell phenotype.

作者信息

Chadwick B S, Miller R G

机构信息

Ontario Cancer Institute, University of Toronto, Canada.

出版信息

Cell Immunol. 1991 Jan;132(1):168-76. doi: 10.1016/0008-8749(91)90016-5.

Abstract

Lymphokine-activated killer cells (LAK) are functionally defined by their ability to mediate the MHC-unrestricted lysis of a range of tumor targets, while sparing normal cells. They can also lyse TNP-modified normal syngeneic lymphoblasts. We show here that lysis of TNP-modified targets is mediated by CD8+ LAK in a self-MHC-restricted manner, whereas lysis of tumor targets is largely by CD8- LAK and is MHC-unrestricted. LAK generated from the immune-deficient strains Balb/c nude and C.B-17 scid lyse tumor targets as effectively as LAK from normal mice but do not lyse TNP-modified normal targets. Further, lysis of TNP-modified targets, but not tumors, can be inhibited by antibody to the T cell receptor complex. These experiments strongly suggest that recognition of TNP-modified targets is not accomplished by the same mechanism as that of tumors. Rather, they are consistent with recognition of TNP-modified targets by CD8+ LAK cells being mediated via recognition through the T cell receptor.

摘要

淋巴因子激活的杀伤细胞(LAK)的功能定义为能够介导对一系列肿瘤靶标的MHC非限制性裂解,同时不损伤正常细胞。它们也能裂解经三硝基苯(TNP)修饰的同基因正常淋巴母细胞。我们在此表明,对TNP修饰靶标的裂解由CD8 + LAK以自身MHC限制性方式介导,而肿瘤靶标的裂解主要由CD8 - LAK介导且不受MHC限制。从免疫缺陷品系Balb/c裸鼠和C.B-17重度联合免疫缺陷小鼠产生的LAK裂解肿瘤靶标的效果与正常小鼠产生的LAK一样,但不能裂解经TNP修饰的正常靶标。此外,针对T细胞受体复合物的抗体可抑制对TNP修饰靶标的裂解,但不能抑制对肿瘤的裂解。这些实验有力地表明,对TNP修饰靶标的识别机制与对肿瘤的识别机制不同。相反,它们与CD8 + LAK细胞对TNP修饰靶标的识别是通过T细胞受体介导的这一观点一致。

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