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淋巴因子激活的杀伤细胞。VII.白细胞介素-4诱导NK1.1⁺CD8α⁺β⁻TCR-αβB220⁺淋巴因子激活的杀伤细胞亚群。

Lymphokine-activated killer cells. VII. IL-4 induces an NK1.1+CD8 alpha+beta- TCR-alpha beta B220+ lymphokine-activated killer subset.

作者信息

Ballas Z K, Rasmussen W

机构信息

Iowa City VA Medical Center, IA.

出版信息

J Immunol. 1993 Jan 1;150(1):17-30.

PMID:7678028
Abstract

Murine IL-2-induced lymphokine-activated killers (LAK) can be divided into two mutually exclusive subsets: NK1.1+CD8- and NK1.1-CD8+. We have previously established that the lytically active subset of each of these two populations expressed B220, as determined by the mAb 6B2, on its surface. In this study, we examined the lytically active subsets induced by IL-4. We found that, similar to IL-2, the lytically active IL-4-LAK expressed B220 on their surface. Similar to IL-2-LAK, IL-4-LAK cultures also contained NK1.1+CD8- B220+, and NK1.1-CD8+B220+ subsets. IL-4-LAK cultures, however, contained two novel and unexpected lymphocyte subsets determined by their surface markers to be either: i) NK1.1+CD8 alpha+beta-B220+, or ii) NK1.1-CD8 alpha+beta-B220+. These subsets were not derived from NK1.1+ or CD8+ precursors but were induced from a CD4-CD8-NK1.1-Slg- splenocyte subpopulation. Most of the CD8 alpha+beta- cells seen in the IL-4 cultures expressed TCR-alpha beta with little or no TCR-gamma delta detected on their surface. Similar to IL-2-LAK, the IL-4-LAK subsets appeared to display a bias as to their susceptible target cells with the NK1.1-CD8 alpha+beta+ subset being most potent against trinitrophenyl-modified autologous lymphoblasts (2,4,6-trinitrobenzene sulfonic acid (TNBS)-self). The NK1.1+CD8 alpha-beta- effectors were most potent against YAC-1 and CL27A with little activity against TNBS-self. All three targets were susceptible to lysis by the NK1.1+CD8 alpha+beta- subset. These findings document the characteristics of a novel lymphocyte subset, derived from splenic precursors, which shares certain features with cells previously thought to be present exclusively in intraepithelial lymphocytes.

摘要

小鼠白细胞介素-2诱导的淋巴因子激活的杀伤细胞(LAK)可分为两个相互排斥的亚群:NK1.1⁺CD8⁻和NK1.1⁻CD8⁺。我们之前已经确定,这两个群体中具有杀伤活性的亚群在其表面表达由单克隆抗体6B2所确定的B220。在本研究中,我们检测了白细胞介素-4诱导的具有杀伤活性的亚群。我们发现,与白细胞介素-2类似,具有杀伤活性的白细胞介素-4-LAK在其表面表达B220。与白细胞介素-2-LAK相似,白细胞介素-4-LAK培养物中也含有NK1.1⁺CD8⁻B220⁺和NK1.1⁻CD8⁺B220⁺亚群。然而,白细胞介素-4-LAK培养物中含有两个新的且出乎意料的淋巴细胞亚群,根据其表面标志物确定为:i)NK1.1⁺CD8α⁺β⁻B220⁺,或ii)NK1.1⁻CD8α⁺β⁻B220⁺。这些亚群并非源自NK1.1⁺或CD8⁺前体细胞,而是由CD4⁻CD8⁻NK1.1⁻Slg⁻脾细胞亚群诱导产生。在白细胞介素-4培养物中看到的大多数CD8α⁺β⁻细胞表达TCR-αβ,在其表面几乎检测不到或没有检测到TCR-γδ。与白细胞介素-2-LAK相似,白细胞介素-4-LAK亚群对其敏感靶细胞似乎表现出偏好,其中NK1.1⁻CD8α⁺β⁺亚群对三硝基苯基修饰的自体淋巴母细胞(2,4,6-三硝基苯磺酸(TNBS)-自身)的杀伤作用最强。NK1.1⁺CD8α⁻β⁻效应细胞对YAC-1和CL27A的杀伤作用最强,对TNBS-自身几乎没有活性。所有三个靶细胞都易被NK1.1⁺CD8α⁺β⁻亚群裂解。这些发现记录了一个源自脾脏前体细胞的新型淋巴细胞亚群的特征,该亚群与先前认为仅存在于上皮内淋巴细胞中的细胞具有某些共同特征。

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