Puddu P, Locardi C, Sestili P, Varano F, Petrini C, Modesti A, Masuelli L, Gresser I, Belardelli F
Laboratory of Virology, Istituto Superiore di Sanità, Rome, Italy.
J Virol. 1991 May;65(5):2245-53. doi: 10.1128/JVI.65.5.2245-2253.1991.
The host factors involved in the restriction of tumor growth were studied in nude mice transplanted with a cloned line of chronically human immunodeficiency virus (HIV)-infected U937 cells. HIV-infected and uninfected U937 cells exhibited the same growth patterns in culture. However, HIV-infected cells were not tumorigenic when injected subcutaneously in nude mice, whereas large solid tumors were observed in mice injected with uninfected U937 cells. Injection of nude mice with antibody to alpha/beta interferon (IFN-alpha/beta) enabled HIV-infected U937 cells to grow progressively in approximately 90 to 100% of mice. HIV-infected U937 cells formed solid tumors in the majority (60 to 90%) of either immunosuppressed (splenectomized, irradiated, and anti-asialo-GM1-treated) or genetically immunodeficient (bg/nu/xid) nude mice. In mice treated with antibodies to IFN-alpha/beta with established HIV-positive tumors, a direct correlation was found between p24 antigenemia and tumor size. Treatment of established HIV-positive U937 cell tumors with human IFN-alpha or mouse IFN-alpha/beta resulted in a clear-cut inhibition of both tumor growth and p24 HIV antigenemia. In contrast, treatment with tumor necrosis factor alpha markedly inhibited tumor growth but did not significantly decrease serum p24 levels. 3'-Azido-3'-deoxythymidine treatment did not affect either tumor growth or the levels of serum p24 antigen. These data indicate that endogenous IFN-alpha/beta is a crucial factor in the restriction of both tumor growth and p24 antigenemia in mice injected with HIV-infected tumor cells. Moreover, the results suggest that the development of HIV-1 p24 antigenemia in athymic immunosuppressed mice may represent an interesting in vivo model for anti-HIV therapy.
在移植了慢性人类免疫缺陷病毒(HIV)感染的U937细胞克隆系的裸鼠中,研究了参与限制肿瘤生长的宿主因素。HIV感染和未感染的U937细胞在培养中表现出相同的生长模式。然而,将HIV感染的细胞皮下注射到裸鼠中时不具有致瘤性,而在注射未感染的U937细胞的小鼠中观察到了大的实体瘤。给裸鼠注射α/β干扰素(IFN-α/β)抗体能使HIV感染的U937细胞在约90%至100%的小鼠中逐渐生长。HIV感染的U937细胞在大多数(60%至90%)免疫抑制(脾切除、照射并经抗唾液酸化GM1处理)或基因免疫缺陷(bg/nu/xid)的裸鼠中形成实体瘤。在用IFN-α/β抗体处理且已形成HIV阳性肿瘤的小鼠中,发现p24抗原血症与肿瘤大小之间存在直接相关性。用人IFN-α或小鼠IFN-α/β处理已形成的HIV阳性U937细胞瘤,可明显抑制肿瘤生长和p24 HIV抗原血症。相比之下,用肿瘤坏死因子α处理可显著抑制肿瘤生长,但并未显著降低血清p24水平。3'-叠氮-3'-脱氧胸苷处理对肿瘤生长或血清p24抗原水平均无影响。这些数据表明,内源性IFN-α/β是限制注射HIV感染肿瘤细胞的小鼠肿瘤生长和p24抗原血症的关键因素。此外,结果表明无胸腺免疫抑制小鼠中HIV-1 p24抗原血症的发展可能是抗HIV治疗的一种有趣的体内模型。