Chakkalath H R, Theodos C M, Markowitz J S, Grusby M J, Glimcher L H, Titus R G
Department of Tropical Public Health, Harvard School of Public Health, Boston, Massachusetts, USA.
J Infect Dis. 1995 May;171(5):1302-8. doi: 10.1093/infdis/171.5.1302.
Class II major histocompatibility complex (MHC)-deficient (H-2b) mice do not express I-A or I-E molecules and, as a result, do not develop CD4 cells. Thus, they represent the ideal model for examining the importance of CD4 cells and MHC class II molecules in resistance to infection with Leishmania major and the capacity of MHC class I-restricted T cells to mediate resistance to L. major. Class II MHC-deficient mice and control (C57BL/6, normal and nude) mice were infected with L. major. Although MHC class II-deficient mice were able to control infection more effectively than nude mice, cutaneous lesions on the mice eventually progressed, and parasite replication became uncontrolled. These results suggest that CD4 cells and MHC class II molecules are essential for resistance to L. major and that in the absence of these cells and molecules, such mice can transiently control infection with L. major but are unable to resolve such infections.
II类主要组织相容性复合体（MHC）缺陷（H-2b）小鼠不表达I-A或I-E分子，因此不会发育出CD4细胞。因此，它们是研究CD4细胞和II类MHC分子在抵抗利什曼原虫感染中的重要性以及I类MHC限制性T细胞介导对利什曼原虫主要种抗性能力的理想模型。将II类MHC缺陷小鼠和对照（C57BL/6，正常和裸鼠）小鼠感染利什曼原虫主要种。尽管II类MHC缺陷小鼠比裸鼠更能有效控制感染，但小鼠的皮肤病变最终仍会进展，并且寄生虫复制变得无法控制。这些结果表明，CD4细胞和II类MHC分子对于抵抗利什曼原虫主要种至关重要，并且在没有这些细胞和分子的情况下，此类小鼠可以暂时控制利什曼原虫主要种的感染，但无法解决此类感染。
