Comparative studies of human FcRIII-positive and negative natural killer cells.
Comparative studies of human FcRIII-positive and negative natural killer cells.
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DOI：
10.4049/jimmunol.143.10.3183
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发表时间：
1989-11
影响因子：
4.4
通讯作者：
A. Nagler;L. Lanier;S. Cwirla;J. Phillips
中科院分区：
文献类型：
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作者：
A. Nagler;L. Lanier;S. Cwirla;J. Phillips
在目前的研究中，我们已经根据CD56和CD16的表面表达鉴定和表征了外周血NK细胞的三个亚群。我们根据CD16的相对表面密度将这些亚群命名为CD16neg， CD16dim和CD16bright。CD16bright亚群约占PBL的10%至15%，而CD16dim和CD16neg亚群占总淋巴细胞的不到1%。对这些子集的详细描述揭示了相似性和差异性。这三个亚群具有大量的表型相似性，在每个亚群中的大多数细胞上表达CD2、CD7、CD11b、CD38、CD45R、CD18和p75 IL-2R。然而，存在一些显著的表型差异，特别是在CD57、CD11c、CD44、CD25、Leu-8、L263和L265的表达方面。cd16阴性细胞在形态学上是大颗粒淋巴细胞，在nk敏感的肿瘤细胞系中表现出低水平的非mhc限制性细胞溶解。CD16dim和CD16bright亚群是大颗粒淋巴细胞，对nk敏感靶点显示出强大的细胞毒性。所有亚群均表现出il -2依赖性激活和增殖；然而，CD16dim和CD16neg亚群优先对极低浓度的il -2有反应。虽然il -4有效抑制了所有三种NK细胞亚群IL-2诱导的细胞溶解激活，但只有CD16bright细胞表现出il -4抑制IL-2依赖性增殖。il -2激活后NK细胞亚群的细胞因子转录也有差异调节。虽然tnf - α在每个亚群中转录相同，但ifn - γ和丝氨酸蛋白酶- hf在cd16亮NK细胞中优先转录。基于这些结果，我们提出这些NK细胞亚群代表了外周血中存在的NK细胞分化途径的一部分。
In the present study we have identified and characterized three subpopulations of peripheral blood NK cells based on the surface expression of CD56 and CD16. We have designated these subsets CD16neg, CD16dim, and CD16bright according to the relative surface density of CD16. The CD16bright subset comprised about 10% to 15% of PBL, whereas the CD16dim and CD16neg subsets comprise less than 1% of the total lymphocytes. A detailed characterization of these subsets revealed both similarities and differences. The three subsets shared a great deal of phenotypic similarity, expressing CD2, CD7, CD11b, CD38, CD45R, CD18, and the p75 IL-2R on the majority of the cells in each subset. There were, however, several prominent phenotypic differences, particularly in the expression of CD57, CD11c, CD44, CD25, Leu-8, L263, and L265. The CD16neg cells were morphologically large agranular lymphocytes and demonstrated low levels of non-MHC restricted cytolysis of NK-sensitive tumor lines. The CD16dim and CD16bright subsets were large granular lymphocytes and revealed potent cytotoxicity against NK-sensitive targets. All subsets demonstrated IL-2-dependent activation and proliferation; however, the CD16dim and CD16neg subsets were preferentially responsive to very low concentrations of rIL-2. Although rIL-4 effectively inhibited the IL-2-induced cytolytic activation of all three NK cell subsets, only the CD16bright cells showed rIL-4 inhibition of IL-2 dependent proliferation. Cytokine transcription was also differentially regulated in the NK cell subsets after rIL-2 activation. Although TNF-alpha was equally transcribed in each subsets, IFN-gamma and serine protease-HF were preferentially transcribed in the CD16bright NK cells. Based on these results, we propose that these NK cell subsets represent portions of the NK cell differentiation pathway present in the peripheral blood.