Notch system in the linkage of innate and adaptive immunity

被引:34
作者
Ito, Toshihiro [1 ]
Connett, Judith M. [2 ]
Kunkel, Steven L. [2 ]
Matsukawa, Akihiro
机构
[1] Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Pathol & Expt Med, Kita Ku, Okayama 7008558, Japan
[2] Univ Michigan, Sch Med, Dept Pathol, Ann Arbor, MI USA
基金
美国国家卫生研究院; 日本学术振兴会;
关键词
antigen-presenting cell (APC); Delta-like; jagged; T cell; infectious model; T-CELL-ACTIVATION; PATHOGEN RECOGNITION; DENDRITIC CELLS; GATA3; EXPRESSION; DIFFERENTIATION; EFFECTOR; LIGAND; SIGNALS; VIRUS; EXPANSION;
D O I
10.1189/jlb.1011529
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The lung is one of the most immunologically challenged organs and can be affected by a number of pathogens, including bacteria, virus, fungi, and parasites. The development and chronicity of pulmonary infection are determined by the early innate response to the pathogenic stimuli and are regulated at multiple levels. Initial studies have indicated that the interaction of Notch and Notch ligands plays a critical role during development, and further, the Notch system is an important bridge between APCs and T cell communication circuits. APCs are essential regulators of the innate immune response. They can respond to PAMPs through PRRs, which function in the recognition of pathogenic components and play an important role in the innate and adaptive immune response. T cells are essential regulators of adaptive immune responses and infectious diseases. However, the role of the Notch system in the cross-talk between APC and T cells during pulmonary infection is still poorly understood. In the present review, we discuss recent findings that explore the mechanisms underlying the role of Notch signaling in the linkage of innate and adaptive immunity, including pulmonary infection though PPRs and Notch activation. J. Leukoc. Biol. 92: 59-65; 2012.
引用
收藏
页码:59 / 65
页数:7
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