IL-1β regulates a novel myeloid-derived suppressor cell subset that impairs NK cell development and function.
IL-1β regulates a novel myeloid-derived suppressor cell subset that impairs NK cell development and function.
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DOI:
10.1002/eji.201041037
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发表时间:
2010-12
影响因子:
5.4
通讯作者:
Vosshenrich, Christian A. J.
中科院分区:
文献类型:
--
作者:
Elkabets, Moshe;Ribeiro, Vera S. G.;Dinarello, Charles A.;Ostrand-Rosenberg, Suzanne;Di Santo, James P.;Apte, Ron N.;Vosshenrich, Christian A. J.
Chronic inflammation is associated with promotion of malignancy and tumor progression. Many tumors enhance the accumulation of myeloid-derived suppressor cells (MDSC), which contribute to tumor progression and growth by suppressing anti-tumor immune responses. Tumor-derived IL-1β secreted into the tumor microenvironment has been shown to induce the accumulation of MDSC possessing an enhanced capacity to suppress T cells. In this study, we found that the enhanced suppressive potential of IL-1β-induced MDSC was due to the activity of a novel subset of MDSC lacking Ly6C expression. This subset was present at low frequency in tumor-bearing mice in the absence of IL-1β-induced inflammation; however, under inflammatory conditions Ly6Cneg MDSC were predominant. Ly6Cneg MDSC impaired NK cell development and functions in vitro and in vivo. These results identify a novel IL-1β-induced subset of MDSC with unique functional properties. Ly6Cneg MDSC mediating NK cell suppression may thus represent useful targets for therapeutic interventions.
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DOI:
10.4049/jimmunol.1000901
发表时间:
2010-08-15
期刊:
Journal of immunology (Baltimore, Md. : 1950)
影响因子:
--
作者:
Lechner MG;Liebertz DJ;Epstein AL
通讯作者:
Epstein AL
影响因子:
5.5
作者:
Bunt, Stephanie K.;Clements, Virginia K.;Ostrand-Rosenberg, Suzanne
通讯作者:
Ostrand-Rosenberg, Suzanne
影响因子:
4.4
作者:
Li, Hequan;Han, Yanmei;Cao, Xuetao
通讯作者:
Cao, Xuetao
影响因子:
20.3
作者:
Movahedi, Kiavash;Guilliams, Martin;Van Ginderachter, Jo A.
通讯作者:
Van Ginderachter, Jo A.
影响因子:
5.4
作者:
De Colvenaer, Veerle;Taveirne, Sylvie;Leclercq, Georges
通讯作者:
Leclercq, Georges