TGF-β affects development and differentiation of human natural killer cell subsets

被引：96

作者：

Allan, David S. J. ^{[1
,2
]}

Rybalov, Basya ^{[1
]}

Awong, Geneve ^{[2
]}

Zuniga-Pfluecker, Juan Carlos ^{[2
]}

Kopcow, Hernan D. ^{[1
]}

Carlyle, James R. ^{[2
]}

Strominger, Jack L. ^{[1
]}

机构：

[1] Harvard Univ, Dept Mol & Cellular Biol, Cambridge, MA 02138 USA

[2] Univ Toronto, Sunnybrook Res Inst, Toronto, ON, Canada

来源：

EUROPEAN JOURNAL OF IMMUNOLOGY | 2010年 / 40卷 / 08期

基金：

加拿大健康研究院; 美国国家卫生研究院;

关键词：

Cell differentiation; Innate immunity; NK cells; GROWTH-FACTOR-BETA; NK CELLS; CD56(BRIGHT); EXPRESSION; CYTOTOXICITY; RECEPTORS; INDUCTION;

D O I：

10.1002/eji.200939910

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

071005 [微生物学]; 100108 [医学免疫学];

摘要：

Human peripheral blood NK cells may be divided into two main subsets: CD56(bright)CD16- and CD56(dim)CD16(+). Since TGF-beta is known to influence the development of many leukocyte lineages, its effects on NK cell differentiation either from human CD34(+)Lin(-) hematopoietic progenitor/stem cells in vitro or from peripheral blood NK cells were investigated. TGF-beta represses development of NK cells from CD34(+) progenitors and inhibits differentiation of CD16(+) NK cells. Moreover, TGF-beta also results in conversion of a minor fraction of CD56(bright)CD16(+) cells found in peripheral blood into CD56(bright)CD16(-) cells, highlighting a possible role of the former as a developmental intermediate and of TGF-beta in influencing the genesis of NK subsets found in blood.

引用

页码：2289 / 2295

页数：7

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