Laboratory of Molecular Immunology, Rega Institute for Medical Research, University of Leuven, Minderbroedersstraat 10, B-3000 Leuven, Belgium.
Immunol Lett. 2012 Jul 30;145(1-2):10-4. doi: 10.1016/j.imlet.2012.04.005.
The arrest and directed migration of leukocytes during homeostasis, tumour development and inflammation is orchestrated by a multitude of chemokines, which govern leukocyte migratory activities. Immune cells are particularly adept at adjusting rapidly to changes within the environment by migration in response to chemokines. The confrontation of leukocytes with different combination of chemokines that are concomitantly produced under physiological or pathological conditions in vivo is complex. There are different ways to enhance or reduce leukocyte migration mediated by chemokines such as posttranslational modifications. Here, we described a positive regulatory mechanism in leukocyte trafficking, by the synergism between chemokines to rapidly augment the local leukocyte influx, thereby enhancing the outcome of an inflammatory response in vivo. The cellular mechanisms involved in chemokine synergy are still debated, but probably include chemokine and/or receptor heterodimerization and subsequent cooperation in signal transduction.
在稳态、肿瘤发展和炎症过程中，白细胞的捕获和定向迁移是由多种趋化因子协调的，这些趋化因子控制着白细胞的迁移活动。免疫细胞特别擅长通过迁移来快速适应环境变化，以响应趋化因子。白细胞与体内生理或病理条件下同时产生的不同组合的趋化因子的对抗是复杂的。有不同的方法可以增强或减少趋化因子介导的白细胞迁移，例如翻译后修饰。在这里，我们描述了一种在白细胞迁移中的正调控机制，即趋化因子之间的协同作用可以迅速增加局部白细胞流入，从而增强体内炎症反应的结果。趋化因子协同作用涉及的细胞机制仍存在争议，但可能包括趋化因子和/或受体异二聚化以及随后在信号转导中的合作。
