Role of Interleukin-12 in Primary Influenza Virus Infection

The effect of endogenous interleukin-12 (IL-12) on the influenza virus immune response in BALB/c mice was evaluated. Following primary influenza virus infection, IL-12 mRNA and protein are detected in the lung, with live virus being required for cytokine induction. Endogenous IL-12 contributes to early NK cell-dependent gamma interferon (IFN-γ) production (days 3 and 5) but not late T-cell-dependent IFN-γ secretion (day 7). IL-12 contributes to the inhibition of early virus replication but is not required for virus clearance. IL-12 also modestly contributes to the activation of cytotoxic T lymphocytes. Thus, in this model of experimental influenza virus infection, endogenous IL-12 contributes primarily to the early development and activation of the innate immune response.

本研究评估了内源性白细胞介素12（interleukin-12, IL-12）对BALB/c小鼠体内流感病毒免疫应答的影响。初次感染流感病毒后，可在肺部检测到IL-12的mRNA与蛋白产物，且细胞因子的诱导需要活病毒参与。内源性IL-12可促进早期依赖自然杀伤细胞（natural killer cell, NK）的γ干扰素（interferon-gamma, IFN-γ）产生（第3天与第5天），但不参与晚期依赖T细胞的IFN-γ分泌（第7天）。IL-12可抑制早期病毒复制，但并非病毒清除所必需。IL-12还可轻度激活细胞毒性T淋巴细胞（cytotoxic T lymphocyte, CTL）。综上，在该实验性流感病毒感染模型中，内源性IL-12主要参与先天免疫应答的早期发育与激活过程。