Lucchiari M A, Pereira C A
Instituto Butantan, Laboratorio de Imunologia Viral, São Paulo, Brasil.
Immunobiology. 1990 Aug;181(1):31-9. doi: 10.1016/S0171-2985(11)80163-4.
In contrast to adult mice, young A/J mice, developed an acute hepatitis following infection with Mouse Hepatitis virus type 3. 100% of the young animals died 4 to 5 days after the infection and high levels of virus were found in the liver and peritoneal exudate. Very low levels of IFN-gamma were found in the serum and peritoneal exudate of infected young mice. This was in contrast to the levels observed in adult mice. Spleen cells and macrophage cultures from young A/J mice, again in contrast to adult A/J mice, were shown to be unable to synthesize IFN-gamma and IFN-alpha/beta respectively. Macrophages from either young or adult A/J mice were able to be activated with exogenous recombinant IFN-gamma or IFN-alpha/beta, enabling both sets of cells to restrict MHV3 replication. The results indicate that the ability of the immune system to synthesize IFN-gamma and IFN-alpha/beta may play a major role in the age-dependent resistance of A/J mice to MHV3.
与成年小鼠不同，幼龄A/J小鼠在感染3型小鼠肝炎病毒后会发生急性肝炎。100%的幼龄动物在感染后4至5天死亡，且在肝脏和腹腔渗出液中发现了高水平的病毒。在受感染幼龄小鼠的血清和腹腔渗出液中发现极低水平的γ干扰素。这与在成年小鼠中观察到的水平形成对比。与成年A/J小鼠再次形成对比的是，幼龄A/J小鼠的脾细胞和巨噬细胞培养物分别无法合成γ干扰素和α/β干扰素。来自幼龄或成年A/J小鼠的巨噬细胞能够被外源性重组γ干扰素或α/β干扰素激活，使两组细胞都能限制MHV3复制。结果表明，免疫系统合成γ干扰素和α/β干扰素的能力可能在A/J小鼠对MHV3的年龄依赖性抗性中起主要作用。
