Baschuk N, Wang N, Watt S V, Halse H, House C, Bird P I, Strugnell R, Trapani J A, Smyth M J, Andrews D M
Cancer Immunology Program, Trescowthick Laboratories, Peter MacCallum Cancer Centre, St. Andrews Place, East Melbourne, Victoria 3002, Australia.
Department of Microbiology and Immunology, The University of Melbourne, Parkville, Victoria 3010, Australia.
Cell Death Dis. 2014 Mar 13;5(3):e1115. doi: 10.1038/cddis.2014.74.
Granzymes are generally recognized for their capacity to induce various pathways of perforin-dependent target cell death. Within this serine protease family, Granzyme M (GrzM) is unique owing to its preferential expression in innate effectors such as natural killer (NK) cells. During Listeria monocytogenes infection, we observed markedly reduced secretion of macrophage inflammatory protein-1 alpha (MIP-1α) in livers of GrzM-deficient mice, which resulted in significantly impaired NK cell recruitment. Direct stimulation with IL-12 and IL-15 demonstrated that GrzM was required for maximal secretion of active MIP-1α. This effect was not due to reduced protein induction but resulted from heightened intracellular accumulation of MIP-1α, with reduced release. These results demonstrate that GrzM is a critical mediator of innate immunity that can regulate chemotactic networks and has an important role in the initiation of immune responses and pathogen control.
颗粒酶通常因其诱导穿孔素依赖性靶细胞死亡的多种途径的能力而被认可。在这个丝氨酸蛋白酶家族中,颗粒酶M(GrzM)是独特的,因为它优先在天然效应细胞如自然杀伤(NK)细胞中表达。在单核细胞增生李斯特菌感染期间,我们观察到GrzM缺陷小鼠肝脏中巨噬细胞炎性蛋白-1α(MIP-1α)的分泌明显减少,这导致NK细胞募集显著受损。用IL-12和IL-15直接刺激表明,GrzM是活性MIP-1α最大分泌所必需的。这种效应不是由于蛋白质诱导减少,而是由于MIP-1α细胞内积累增加,释放减少。这些结果表明,GrzM是先天免疫的关键介质,可调节趋化网络,并在免疫反应的启动和病原体控制中起重要作用。