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聚腺苷酸-聚尿苷酸(聚A:U)与实验性小鼠布鲁氏菌病。II. 巨噬细胞作为实验性布鲁氏菌病中聚A:U的靶细胞

Polyadenylic acid-polyuridylic acid (poly A : U) and experimental murine brucellosis. II. Macrophages as target cells of poly A : U in experimental brucellosis.

作者信息

Madraso E D, Cheers C

出版信息

Immunology. 1978 Jul;35(1):77-84.

Abstract

Results of and experiments suggest that the early suppression of brucella growth in double stranded polyadenylic-polyuridylic acid-(poly A:U-) treated mice was due to a non-specific activation of macrophages by poly A:U. Poly A:U administered intraperitoneally at the time of brucella infection failed to enhance T-cell mediated responses to the organism, namely delayed-type hyper-sensitivity to brucellin and adoptive transfer of immunity to the infection. Poly A:U did not augment the protective antibodies formed in response to infection. Although poly A:U has been previously found to suppress brucellosis in athymic (nude) mice, it did not enhance the thymus-dependent antibody response to sheep erythrocytes in brucella-infected nudes, suggesting that it did not significantly enhance maturation of their helper T-cell percursors. Increased macrophage spreading, an indication of activation, was seen immediately after administration of poly A:U and . Later on the infection spreading was suppressed, a phenomenon which appears to relate to the biphasic effect of poly A:U described in the accompanying paper. Peritoneal macrophages treated with poly A:U were stimulated to spread on plastic surfaces, even when T lymphocytes were removed with anti-Thy-1 serum and complement.

摘要

实验结果表明,在双链聚腺苷酸-聚尿苷酸(聚A:U)处理的小鼠中,布鲁氏菌生长的早期抑制是由于聚A:U对巨噬细胞的非特异性激活。在布鲁氏菌感染时腹腔注射聚A:U未能增强T细胞介导的对该病原体的反应,即对布鲁氏菌素的迟发型超敏反应和对感染的免疫过继转移。聚A:U并未增强因感染而形成的保护性抗体。尽管先前已发现聚A:U可抑制无胸腺(裸)小鼠的布鲁氏菌病,但它并未增强布鲁氏菌感染的裸鼠对绵羊红细胞的胸腺依赖性抗体反应,这表明它并未显著增强其辅助性T细胞前体的成熟。给药聚A:U后立即观察到巨噬细胞铺展增加,这是激活的一个指标。随后感染的扩散受到抑制,这一现象似乎与随附论文中描述的聚A:U的双相效应有关。用聚A:U处理的腹腔巨噬细胞即使在用抗Thy-1血清和补体去除T淋巴细胞后仍能在塑料表面铺展。

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