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Host defenses in murine malaria: analysis of the mechanisms of immunity to Plasmodium berghei generated in response to immunization with formalin-killed blood-stage parasites.

机译:鼠类疟疾的宿主防御:分析对福尔马林杀死的血期寄生虫免疫后产生的对伯氏疟原虫免疫的机制。

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Syngeneic B6D2F1 (C57Bl/6 x DBA/2) mice were immunized with a nonliving antigen prepared from mixed blood forms of Plasmodium berghei strain NYU-2. Consistently greater than 80% of the vaccinated mice survived virulent challenge, and protective immunity was demonstrable from 1 week through at least 4 months after immunization. However, vaccination did not prevent the development of patient infection after challenge. Instead, infections in vaccinated mice progressed to about 10% parasitemia and were then subsequently cleared. In contrast, infections initiated in nonvaccinated mice progressed beyond 10% parasitemia and were uniformly fatal within 4 weeks. Sera collected from normal mice, nonvaccinated mice infected with P. berghei, or vaccinated mice before challenge failed to passively protect recipients against virulent infection. On the other hand, sera collected from vaccinated mice after recovery from a challenge infection conferred upon passively immunized recipients protection from homologous virulent challenge, which was manifest as a delay in the onset of overt infection. It was concluded, therefore, that vaccination altered the immunological potential of the host in such a way as to allow the production of a protective humoral factor, probably specific antibody, in response to infection with the virulent parasites.
机译:用由伯氏疟原虫菌株NYU-2的混合血液形式制备的无生命抗原免疫同基因B6D2F1(C57Bl / 6 x DBA / 2)小鼠。始终有超过80%的疫苗接种小鼠在毒性攻击后存活,并且在免疫后1周到至少4个月可证明有保护性免疫。但是,接种疫苗并不能阻止挑战后患者感染的发展。取而代之的是,接种疫苗的小鼠中的感染发展为约10%的寄生虫血症,随后被清除。相反,在未接种疫苗的小鼠中开始的感染进展为寄生虫病超过10%,并且在4周内均匀致死。从正常小鼠,感染伯氏疟原虫的未接种疫苗的小鼠或攻击前接种的小鼠收集的血清不能被动地保护受体免受强毒感染。另一方面,从攻击性感染恢复后从接种的小鼠中收集的血清赋予被动免疫的接受者免受同源毒性攻击的保护,这表现为明显感染发作的延迟。因此,可以得出结论,接种疫苗以某种方式改变了宿主的免疫潜能,从而使得能够响应于感染有毒的寄生虫而产生保护性体液因子,可能是特异性抗体。

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