PKC-θ function at the immunological synapse: prospects for therapeutic targeting

被引：60

作者：

Zanin-Zhorov, Alexandra ^{[3
]}

Dustin, Michael L. ^{[3
]}

Blazar, Bruce R. ^{[1
,2
]}

机构：

[1] Univ Minnesota, Ctr Canc, Minneapolis, MN 55455 USA

[2] Univ Minnesota, Dept Pediat, Div Blood & Marrow Transplantat, Minneapolis, MN 55455 USA

[3] NYU, Sch Med, Mol Pathogenesis Program,Skirball Inst Biomol Med, Helen & Martin Kimmel Ctr Biol & Med,Dept Pathol, New York, NY 10016 USA

来源：

TRENDS IN IMMUNOLOGY | 2011年 / 32卷 / 08期

关键词：

KINASE-C-THETA; REGULATORY T-CELLS; NF-KAPPA-B; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; IN-VIVO; TRANSCRIPTION FACTOR; DEFICIENT MICE; ACTIVATION; RECEPTOR; RESPONSES;

D O I：

10.1016/j.it.2011.04.007

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Protein kinase C (PKC)-theta regulates conventional effector T (Teff) cell function. Since this initial finding, it has become clear that the role of PKC-theta in T cells is complex. PKC-theta plays a central role in Teff cell activation and survival, and negatively regulates stability of the immunological synapse (IS). Recent studies demonstrated that PKC-theta is required for the development of natural CD4(+)Foxp3(+) regulatory T (Treg) cells, and mediates negative regulation of Treg cell function. Here, we examine the role of PKC-theta in the IS, evidence for its distinct localization in Treg cells and the therapeutic implications of inhibiting PKC-theta in Teff cells, to reduce effector function, and in Treg cells, to increase suppressor function, for the prevention and treatment of autoimmune and alloimmune disease states.

引用

页码：358 / 363

页数：6

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