用刚地弓形虫感染小鼠巨噬细胞与转化生长因子β的释放及肿瘤坏死因子受体表达的下调有关。
Infection of murine macrophages with Toxoplasma gondii is associated with release of transforming growth factor beta and downregulation of expression of tumor necrosis factor receptors.
作者信息
Bermudez L E, Covaro G, Remington J
机构信息
Kuzell Institute of Arthritis and Infectious Diseases, Medical Research Institute of San Francisco, California Pacific Medical Center 94115.
出版信息
Infect Immun. 1993 Oct;61(10):4126-30. doi: 10.1128/iai.61.10.4126-4130.1993.
Abstract
Toxoplasma gondii is capable of invading and multiplying within murine peritoneal macrophages. Previous studies have shown that treatment of macrophage monolayers with recombinant gamma interferon but not tumor necrosis factor (TNF) is associated with intracellular killing of T. gondii by macrophages. Furthermore, infection of macrophages with T. gondii prevents their stimulation for mycobactericidal activity by TNF. Since transforming growth factor beta (TGF-beta) is known to suppress a number of functions in macrophages, we investigated the influence of infection with T. gondii on macrophage TNF receptors and on production of TGF-beta. Infection with T. gondii was associated with increased production of TGF-beta and downregulation of TNF receptors. This effect was observed early after infection and was partially inhibited by anti-TGF-beta 1 antibody.
摘要
刚地弓形虫能够在小鼠腹腔巨噬细胞内侵入并繁殖。先前的研究表明，用重组γ干扰素而非肿瘤坏死因子（TNF）处理巨噬细胞单层与巨噬细胞对刚地弓形虫的细胞内杀伤作用有关。此外，刚地弓形虫感染巨噬细胞会阻止其被TNF刺激产生杀分枝杆菌活性。由于已知转化生长因子β（TGF-β）会抑制巨噬细胞的多种功能，我们研究了刚地弓形虫感染对巨噬细胞TNF受体以及TGF-β产生的影响。刚地弓形虫感染与TGF-β产生增加和TNF受体下调有关。这种效应在感染后早期即可观察到，并且被抗TGF-β1抗体部分抑制。
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