Brenan M, Zinkernagel R M
Infect Immun. 1983 Aug;41(2):470-5. doi: 10.1128/iai.41.2.470-475.1983.
The influence of one virus on the in vivo cytotoxic T-cell response to a different concurrent viral infection was analyzed. Lymphocytic choriomeningitis and Newcastle disease viruses, known to induce high interferon titers, and the synthetic interferon inducer polyriboinosinic acid-polyribocytidylic acid inhibited the cytotoxic T-cell response against the second virus. In contrast, vaccinia and vesicular stomatitis viruses failed to induce inhibition. Inhibition directly correlated with the interferon titers; similarly, the interferon titers directly correlated with macrophage and natural killer cell activation. The involvement in vivo of interferon in macrophage and natural killer cell activation and the possible mechanisms of inhibition of the cytotoxic responses are shown by the inhibition of the effect by antibodies against interferon.
分析了一种病毒对针对另一种同时发生的病毒感染的体内细胞毒性T细胞反应的影响。已知能诱导高干扰素滴度的淋巴细胞性脉络丛脑膜炎病毒和新城疫病毒,以及合成干扰素诱导剂聚肌苷酸-聚胞苷酸抑制了针对第二种病毒的细胞毒性T细胞反应。相比之下,痘苗病毒和水疱性口炎病毒未能诱导抑制作用。抑制作用与干扰素滴度直接相关;同样,干扰素滴度与巨噬细胞和自然杀伤细胞的激活直接相关。抗干扰素抗体对这种效应的抑制表明了干扰素在体内参与巨噬细胞和自然杀伤细胞的激活以及细胞毒性反应抑制的可能机制。