β干扰素在抗弓形虫感染中的作用。
Role of beta interferon in resistance to Toxoplasma gondii infection.
作者信息
Orellana M A, Suzuki Y, Araujo F, Remington J S
机构信息
Department of Immunology & Infectious Diseases, Palo Alto Medical Foundation, California 94301.
出版信息
Infect Immun. 1991 Sep;59(9):3287-90. doi: 10.1128/iai.59.9.3287-3290.1991.
The role of recombinant murine beta interferon (rMuIFN-beta) and recombinant human IFN-beta (rHuIFN-beta) in resistance to Toxoplasma gondii was examined. rMuIFN-beta protected mice against a lethal infection with the parasite. The protective effect appeared to depend on the concomitant release of gamma interferon. rMuIFN-beta did not activate murine peritoneal macrophages to inhibit or kill T. gondii whether used alone or in combination with lipopolysaccharide (LPS). rHuIFN-beta did not activate human monocyte-derived macrophages to inhibit or kill T. gondii when 5-day-old monocyte-derived macrophages were used. In contrast, significant killing of T. gondii was noted when 10-day-old monocyte-derived macrophages were used. The addition of LPS enhanced this effect. These results revealed a role for IFN-beta in the mechanisms of defense against T. gondii and suggest its potential use in the treatment of toxoplasmosis in humans.
研究了重组鼠β干扰素（rMuIFN-β）和重组人干扰素-β（rHuIFN-β）在抗弓形虫感染中的作用。rMuIFN-β可保护小鼠免受该寄生虫的致死性感染。其保护作用似乎依赖于γ干扰素的同时释放。单独使用rMuIFN-β或与脂多糖（LPS）联合使用时，均不能激活鼠腹膜巨噬细胞来抑制或杀死弓形虫。当使用5日龄单核细胞衍生巨噬细胞时，rHuIFN-β不能激活人单核细胞衍生巨噬细胞来抑制或杀死弓形虫。相反，当使用10日龄单核细胞衍生巨噬细胞时，可观察到对弓形虫的显著杀伤作用。添加LPS可增强这种作用。这些结果揭示了IFN-β在抗弓形虫防御机制中的作用，并提示其在治疗人类弓形虫病中的潜在用途。
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