Freudenberg Marina A, Merlin Thomas, Kalis Christoph, Chvatchko Yolande, Stübig Hella, Galanos Chris
Max-Planck-Institut für Immunbiologie, Freiburg, Germany.
J Immunol. 2002 Aug 15;169(4):1665-8. doi: 10.4049/jimmunol.169.4.1665.
IFN-alphabeta is a potent immunoregulatory cytokine involved in the defense against viral and bacterial infections. In this study, we describe an as yet undefined IFN-alphabeta-dependent pathway of IFN-gamma induction in mice. This pathway is based on a synergism of IFN-alphabeta and IL-18, and is independent of IL-12 signaling yet dependent on STAT4. In contradiction to current dogma, we show further that IFN-alphabeta alone induces tyrosine phosphorylation of STAT4 in murine splenocytes of different mouse strains. This pathway participates in the induction of IFN-gamma by Gram-negative bacteria and is therefore expected to play a role whenever IFN-alpha or IFN-beta and IL-18 are produced concomitantly during bacterial, viral, or other infections.
干扰素αβ是一种强效免疫调节细胞因子，参与抵御病毒和细菌感染。在本研究中，我们描述了小鼠中一种尚未明确的依赖干扰素αβ的干扰素γ诱导途径。该途径基于干扰素αβ与白细胞介素18的协同作用，独立于白细胞介素12信号传导但依赖于信号转导和转录激活因子4（STAT4）。与当前的观点相反，我们进一步表明，单独的干扰素αβ可诱导不同小鼠品系的小鼠脾细胞中STAT4的酪氨酸磷酸化。该途径参与革兰氏阴性菌诱导的干扰素γ的产生，因此预计在细菌、病毒或其他感染过程中，只要同时产生干扰素α或干扰素β和白细胞介素18，该途径就会发挥作用。
