Murphy J R, Wisseman C G, Fiset P
Infect Immun. 1979 May;24(2):387-93. doi: 10.1128/iai.24.2.387-393.1979.
When nonimmune guinea pigs are inoculated intradermally (i.d.) with Rickettsia mooseri (R. typhi), the rickettsiae replicate at the site of inoculation, leading to the development of a grossly observable lesion. In contrast, guinea pigs which have recovered from R. mooseri infection are resistant to challenge and prevent both rickettsial growth and the formation of lesions. To study the mechanisms of this immunity, sera or splenic cells collected from nonimmune or immune guinea pigs were inoculated separetely into nonimmune recipients. Splenic cells collected from immune donors protected R. mooseri-naive recipients from i.d. challenge as measured by control of rickettsial growth and by prevention of development of lesions at i.d. sites of inoculation. In contrast, serum from immune and nonimmune doners failed to protect nonimmune recipients by either criterion.
当用莫氏立克次体(斑疹伤寒立克次体)对未免疫的豚鼠进行皮内接种时,立克次体在接种部位复制,导致出现肉眼可见的病变。相比之下,从莫氏立克次体感染中恢复的豚鼠对再次攻击具有抗性,可阻止立克次体生长和病变形成。为研究这种免疫的机制,将从未免疫或免疫豚鼠收集的血清或脾细胞分别接种到未免疫的受体中。从免疫供体收集的脾细胞可保护未接触过莫氏立克次体的受体免受皮内攻击,这可通过控制立克次体生长以及预防接种部位皮内病变的发展来衡量。相比之下,无论按照哪种标准,来自免疫和未免疫供体的血清均无法保护未免疫的受体。