Kolosov M, Kolosova I, Zhou A, Leu R W
Oklahoma Medical Research Foundation, Noble Center for Biomedical Research, Oklahoma City 73104-5046, USA.
J Interferon Cytokine Res. 1996 Mar;16(3):209-15. doi: 10.1089/jir.1996.16.209.
Peritoneal macrophages (M phi) constitutively synthesize and secrete interferon-alpha (IFN-alpha) and IFN-beta, as well as complement subcomponent C1q. Because exogenous interferon-gamma (IFN-gamma) stimulates Mø synthesis of C1q, our purpose was to determine if endogenous secretion of IFN-alpha/beta regulated the constitutive level of endogenous C1q mRNA synthesis in an autocrine fashion. Both exogenous IFN-alpha and IFN-beta effectively substituted for IFN-gamma in stimulating M phi C1q mRNA expression in a dose-dependent fashion by northern blot analysis. Neutralizing anti-INF-alpha/beta antibodies inhibited M phi constitutive C1q mRNA synthesis by approximately twofold and abrogated the feedback stimulatory effects of exogenous C1q on C1q mRNA expression. Paraffin oil-elicited inflammatory M phi displayed distinctively different constitutive levels of C1q mRNA expression from thioglycollate brothelicited M phi, which was correlated with their relative levels of secretory IFN-alpha/beta by ELISA. Exogenous IFN-alpha/beta also restored C1q mRNA synthesis of AKR mouse M phi with low constitutive C1q mRNA expression. The cumulative results support the concept that constitutive synthesis of C1q by M phi is regulated by the endogenous synthesis and secretion of IFN-alpha/beta, which appears to act in an autocrine fashion.
腹膜巨噬细胞（M phi）可组成性地合成和分泌α干扰素（IFN-α）、β干扰素（IFN-β）以及补体亚成分C1q。由于外源性γ干扰素（IFN-γ）可刺激Mø合成C1q，我们的目的是确定内源性α/β干扰素的分泌是否以自分泌方式调节内源性C1q mRNA合成的组成水平。通过Northern印迹分析，外源性α干扰素和β干扰素均可有效替代γ干扰素，以剂量依赖性方式刺激M phi C1q mRNA表达。中和性抗IFN-α/β抗体可抑制M phi组成性C1q mRNA合成约两倍，并消除外源性C1q对C1q mRNA表达的反馈刺激作用。石蜡油诱导的炎性M phi与巯基乙酸肉汤诱导的M phi相比，显示出明显不同的C1q mRNA表达组成水平，这与通过ELISA检测的它们的分泌性IFN-α/β相对水平相关。外源性IFN-α/β还可恢复组成性C1q mRNA表达水平较低的AKR小鼠M phi的C1q mRNA合成。累积结果支持这样的概念，即M phi组成性合成C1q受IFN-α/β的内源性合成和分泌调节，这似乎以自分泌方式起作用。
