Experimental malaria in the CBA/N mouse.
Experimental malaria in the CBA/N mouse.
复制标题
CBA/N 小鼠的实验性疟疾。
DOI：
10.4049/jimmunol.123.6.2532
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发表时间：
1979
影响因子：
4.4
通讯作者：
J. Kemp
中科院分区：
文献类型：
--
作者：
A. Jayawardena;C. Janeway;J. Kemp
CBA/N小鼠携带X-连锁隐性基因，其导致B细胞亚群的缺失，并且主要表现为不能对某类胸腺非依赖性抗原应答。我们已经检查了这些小鼠对疟疾寄生虫约氏疟原虫的反应，发现这种寄生虫引起的原发感染在X连锁缺陷小鼠中比正常对照组更严重，持续时间更长。缺陷小鼠的抵抗力下降与其IgM抗体反应的显著缺陷有关。从初次感染中恢复后，缺陷小鼠与正常小鼠一样抵抗同源寄生虫的再次感染。尽管与正常对照一样具有抵抗力，但与正常动物的B细胞相比，来自缺陷小鼠的B细胞向初始受体转移的免疫力要少得多。因此，两种胸腺依赖的保护性免疫模式可能有助于宿主对约氏疟原虫的应答。急性原发感染的控制似乎涉及CBA/N小鼠缺乏的胸腺依赖性抗体应答。对再感染的抵抗可能主要由不同的机制介导。
CBA/N mice carry an X-linked, recessive gene, which results in the absence of a B cell subset, and is expressed primarily as an inability to respond to a certain class of thymus-independent antigens. We have examined the responses of these mice to the malaria parasite Plasmodium yoelii and found that primary infections induced by this parasite are more severe and last longer in mice with X-linked defect than in normal controls. The decreased resistance of the defective mice is associated with a striking deficiency in their IgM antibody response. After recovery from a primary infection, defective mice resist reinfection with the homologous parasite as well as normal mice. Although as resistant as normal controls, B cells from defective mice transfer considerably less immunity to naive recipients than B cells from normal animals. Hence, two modes of thymus-dependent protective immunity may contribute to the host response to P. yoelii. Control of an acute primary infection appears to involve a thymus-dependent antibody response that CBA/N mice are deficient in. Resistance to reinfection may be mediated primarily by a different mechanism.