聚肌胞苷酸诱导的干扰素增强CB-17小鼠对系统性念珠菌病的易感性
Enhancement of susceptibility of CB-17 mice to systemic candidiasis by poly(I . C)-induced interferon.
作者信息
Jensen J, Balish E
机构信息
Department of Surgery, University of Wisconsin Medical School, Madison 53706.
出版信息
Infect Immun. 1993 Aug;61(8):3530-2. doi: 10.1128/iai.61.8.3530-3532.1993.
Abstract
Poly(I . C) enhanced the susceptibility of CB-17 (BALB/c) mice to acute systemic candidiasis. Poly(I . C), supernatants from poly(I . C)-treated macrophages, or alpha and beta interferons suppressed macrophage candidacidal activity in vitro. Thus, poly(I . C)-induced interferons may enhance the susceptibility of CB-17 mice to candidiasis by suppressing macrophage candidacidal activity in an autocrine fashion.
摘要
聚肌胞苷酸（Poly(I.C)）增强了CB - 17（BALB/c）小鼠对急性全身性念珠菌病的易感性。聚肌胞苷酸、经聚肌胞苷酸处理的巨噬细胞的上清液，或α和β干扰素在体外均可抑制巨噬细胞的杀念珠菌活性。因此，聚肌胞苷酸诱导产生的干扰素可能通过以自分泌方式抑制巨噬细胞的杀念珠菌活性，从而增强CB - 17小鼠对念珠菌病的易感性。
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