Pesce Silvia, Moretta Lorenzo, Moretta Alessandro, Marcenaro Emanuela
Dipartimento di Medicina Sperimentale, Università degli Studi di Genova , Genova , Italy.
Dipartimento di Immunologia, IRCCS Bambino Gesù Ospedale Pediatrico , Rome , Italy.
Front Immunol. 2016 Oct 7;7:414. doi: 10.3389/fimmu.2016.00414. eCollection 2016.
Innate and adaptive immunity has evolved complex molecular mechanisms regulating immune cell migration to facilitate the dynamic cellular interactions required for its function involving the chemokines and their receptors. One important chemokine receptor in the immune system is represented by CCR7. Together with its ligands CCL19 and CCL21, this chemokine receptor controls different arrays of migratory events, both in innate and adaptive immunity, including homing of CD56 NK cells, T cells, and DCs to lymphoid compartments, where T cell priming occurs. Only recently, a key role for CCR7 in promoting CD56 NK cell migration toward lymphoid tissues has been described. Remarkably, this event can influence the shaping and polarization of adaptive T cell responses. In this review, we describe recent progress in understanding the mechanisms and the site where CD56 KIR NK cells can acquire the capability to migrate toward lymph nodes. The emerging significance of this event in clinical transplantation is also discussed.
先天性免疫和适应性免疫已经进化出复杂的分子机制来调节免疫细胞迁移,以促进其功能所需的动态细胞相互作用,这涉及趋化因子及其受体。免疫系统中的一种重要趋化因子受体是CCR7。该趋化因子受体与其配体CCL19和CCL21一起,控制先天性免疫和适应性免疫中不同的迁移事件,包括CD56自然杀伤(NK)细胞、T细胞和树突状细胞(DC)归巢至发生T细胞致敏的淋巴区室。直到最近,才有人描述CCR7在促进CD56 NK细胞向淋巴组织迁移中起关键作用。值得注意的是,这一事件可影响适应性T细胞反应的形成和极化。在本综述中,我们描述了在理解CD56杀伤细胞免疫球蛋白样受体(KIR)NK细胞获得向淋巴结迁移能力的机制和部位方面的最新进展。还讨论了这一事件在临床移植中的新意义。