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目的分析IL-2的抗弓形虫作用,并探讨其机制.方法采用3H一尿嘧淀(3H-U)特异性标记弓形虫在小鼠腹腔巨噬细胞(MOUSEPERITONEALMACROPHAGEMPM)内的增殖实验及125I-UDR标记的细胞毒实验,观察IL-2在小鼠抗弓形虫中的作用.结果体外应用IL-2对MPM抗弓形虫作用无影响,体内应用IL-2能明显延长急性弓形虫感染小鼠的生存时间(P＜0.05).IL-2治疗组小鼠脾细胞杀伤肿瘤细胞及弓形虫感染自身靶细胞的能力,明显高于对照组(P＜O.001);正常小鼠NK细胞及LAK细胞杀伤自身感染弓形虫靶细胞的能力,显著低于杀伤肿瘤细胞的能力(P＜0.001);IL-2诱导的LAK细胞杀伤自身感染弓形上靶细胞的能力,明显高于NK细胞(P＜0.001),且与LAK细胞杀伤肿瘤靶细胞的能力无明显差别.结论以上结果表明,IL-2体内应用提高弓形虫感染小鼠生存能力的机制,可能与提高体内LAK细胞杀伤自身感染弓形虫靶细胞的能力有关;NK细胞的抗弓形虫机制,可能在于激活NK细胞产生IFNΓ和TNFΑ等细胞因子,间接作用于巨噬细胞而发挥作用.“,”AIM Experiments were conducted to determine whether mouse lymphokine activated killer(LAK) cells arecytotoxic against cells infected with toxoplasma gondii. METHODS and RESULTS In vitro,IL-2 did not induce the toxoplasmastatic activityof MPM. IL-2 in combination with variousconcentrationsof IFN did not enhance these effectorfunctions morethan IFNγ alone. However in vivotreatment of micewith 700u IL-2 had prolonged time of survival compared with contral mice affer infection with 1 * 102 tachyzoites of RH strain(P<0. 005 ). Studies on the protective mechanism demonstrated that IL-2 could signigicantly enhanc the NK and LAK activity to kill tumor target cells and LAK activity to kill autologeus spleen cells infected with toxoplasma gondii but not NK activity. CONCLUSION Our results in vitro and in vivo suggest adminstration of LAK cells might prove of therapeutic use in immunocompromised patients.