Kitaura M, Kato T, Inaba K, Watanabe Y, Kawade Y, Muramatsu S
Department of Zoology, Faculty of Science, Kyoto University, Japan.
Dev Comp Immunol. 1988 Summer;12(3):645-55. doi: 10.1016/0145-305x(88)90080-8.
Peritoneal exudate macrophages (M phi) of newborn mice (NB-M phi) were apparently almost incapable of expressing Ia antigen even if stimulated by IFN-gamma. No significant difference was observed in the number and the affinity of receptors for IFN-gamma between NB-M phi and M phi of adult mice (Ad-M phi). Addition of indomethacin, a prostaglandin synthesis inhibitor, was ineffective in enhancing the Ia-expression of NB-M phi. Responsiveness of NB-M phi to IFN-gamma, however, was disclosed by the addition to the culture of anti-IFN-beta or anti-IFN-alpha/beta, but not anti-IFN-alpha antibody. Responsiveness of NB-M phi to IFN-gamma was not improved by the depletion of fibroblasts from NB-M phi populations. These results strongly argue that Ia-expression of NB-M phi, which is otherwise to be induced by IFN-gamma, is suppressed by IFN-beta derived from NB-M phi themselves.
新生小鼠的腹腔渗出巨噬细胞(M phi)(NB-M phi)即使受到γ干扰素刺激,显然几乎无法表达Ia抗原。在NB-M phi和成年小鼠的M phi(Ad-M phi)之间,γ干扰素受体的数量和亲和力未观察到显著差异。添加前列腺素合成抑制剂消炎痛对增强NB-M phi的Ia表达无效。然而,通过在培养物中添加抗β干扰素或抗α/β干扰素(而非抗α干扰素抗体),可揭示NB-M phi对γ干扰素的反应性。从NB-M phi群体中去除成纤维细胞并不能改善NB-M phi对γ干扰素的反应性。这些结果有力地表明,原本可由γ干扰素诱导的NB-M phi的Ia表达受到NB-M phi自身产生的β干扰素的抑制。