γ干扰素对单核吞噬细胞恶病质素表达的影响。内毒素耐受（Lpsd）表型的逆转。
Effect of gamma interferon on cachectin expression by mononuclear phagocytes. Reversal of the lpsd (endotoxin resistance) phenotype.
作者信息
Beutler B, Tkacenko V, Milsark I, Krochin N, Cerami A
出版信息
J Exp Med. 1986 Nov 1;164(5):1791-6. doi: 10.1084/jem.164.5.1791.
Abstract
IFN-gamma permits the endotoxin-induced production of cachectin by C3H/HeJ (endotoxin resistant) macrophages, apparently by facilitating endotoxin-induced cachectin biosynthesis at both transcriptional and posttranscriptional levels. IFN-gamma cannot induce cachectin biosynthesis by itself, nor does it markedly enhance cachectin production by endotoxin-induced peritoneal macrophages obtained from endotoxin-responsive mice. Elucidation of the precise mechanism through which IFN-gamma influences cachectin biosynthesis may permit a better understanding of the molecular events that follow endotoxin-induced activation of macrophages. Moreover, the permissive effect of IFN-gamma on cachectin biosynthesis might elicit enhanced endotoxin sensitivity in vivo.
摘要
γ干扰素可使C3H/HeJ（对内毒素耐受）巨噬细胞产生内毒素诱导的恶病质素，这显然是通过在转录和转录后水平促进内毒素诱导的恶病质素生物合成来实现的。γ干扰素本身不能诱导恶病质素的生物合成，对于从对内毒素敏感的小鼠获得的内毒素诱导的腹腔巨噬细胞，它也不会显著增强恶病质素的产生。阐明γ干扰素影响恶病质素生物合成的确切机制，可能有助于更好地理解内毒素诱导巨噬细胞活化后发生的分子事件。此外，γ干扰素对恶病质素生物合成的允许作用可能会引起体内对内毒素敏感性的增强。
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