抗菌蛋白颗粒蛋白(GNLY)是由活化的人细胞毒性T淋巴细胞(CTL)和自然杀伤细胞(NK)分泌的(Pena SV et al. 1997;Stenger S et al. 1998;Hanson DA et al. 1999;Ogawa K et al. 2003)。阳离子GNLY结合在细菌中发现的带负电荷的表面，导致细胞外和细胞内病原体的膜缺陷(Stenger S et al. 1998;Ernst WA et al. 2000;Barman H et al. 2006)。虽然GNLY表现出较强的抗菌活性，但它不能透过含有真核脂质成分的细胞膜(Barman H et al. 2006)。GNLY结合真核细胞膜上的脂筏或磷脂，可被脂筏内化并传递到早期的分选核内体，这些核内体随后与含细菌的吞噬体融合，从而诱导GNLY介导的细菌裂解(Walch M et al. 2005, 2007)。GNLY可能需要穿孔素作为辅助因子进入宿主细胞(Stenger S et al. 1998)。 it was also suggested that perforin promotes GNLY-mediated bacteriolysis not by the formation of stable pores that allow passive diffusion of GNLS but rather by an increase in endosome-phagosomes fusion triggered by an intracellular Ca(2+) rise (Walch M et al. 2007).