Identification of human NK cells that are deficient for signaling adaptor FcRγ and specialized for antibody-dependent immune functions

白细胞介素21 Janus激酶3 生物 CD16 脱颗粒 细胞生物学 白细胞介素12 淋巴因子激活杀伤细胞 抗体 细胞因子 Fc受体 CD49b 受体 NK-92 免疫系统 细胞毒性T细胞 免疫学 分子生物学 CD3型 T细胞 CD8型 体外 生物化学
作者
Ilwoong Hwang,Tianxiang Zhang,Jeannine M. Scott,Ae Ra Kim,Taehyung Lee,Tejaswi Kakarla,Ahrom Kim,John B. Sunwoo,Sung‐Jin Kim
出处
期刊:International Immunology [Oxford University Press]
卷期号:24 (12): 793-802 被引量:158
标识
DOI:10.1093/intimm/dxs080
摘要

Abstract NK cells respond to tumor and virus-infected cells directly through several activation receptors, including natural cytotoxicity receptors, or indirectly through the activating Fc receptor CD16 for antibody-coated cells. Triggering of NK-cell effector functions through these receptors depends on physically associated transmembrane signaling adaptors, such as FcRγ (also known as FcεRIγ) and CD3ζ, both of which have been traditionally believed to be expressed by all mature NK cells. However, we have identified a distinct subset of human NK cells that are deficient for FcRγ expression but express normal levels of CD3ζ. FcRγ-deficient NK cells were readily detectable in about one-third of the healthy individuals examined. The deficiency was confined to the CD56dim population and was due to low FcRγ mRNA. FcRγ-deficient NK cells displayed dramatically reduced expression of the natural cytotoxicity receptors NKp46 and NKp30 but still expressed substantial levels of CD16. Compared to FcRγ-expressing NK cells, FcRγ-deficient NK cells showed poor direct reactivity toward tumor targets as measured by cytokine production and degranulation. Unexpectedly, however, FcRγ-deficient NK cells exhibited significantly more robust responsiveness upon stimulation through CD16, particularly for cytokine production, compared to FcRγ-expressing NK cells. Thus, our study reveals FcRγ-deficient NK cells as a novel subset of human NK cells that have remarkably potent responses toward antibody-coated targets. These findings also illustrate a differential contribution of FcRγ and CD3ζ for the expression and functional activity of their associated receptors.

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