van der Heyde H C, Elloso M M, Chang W L, Kaplan M, Manning D D, Weidanz W P
Department of Medical Microbiology and Immunology, University of Wisconsin, Madison 53706, USA.
J Immunol. 1995 Apr 15;154(8):3985-90.
To determine whether gamma delta T cells are essential for the resolution of acute Plasmodium chabaudi adami (P. c. adami) malaria, we depleted gamma delta T cells from C57BL/6 mice with hamster monoclonal anti-TCR gamma delta Ab treatment. During the period in which control mice that had received normal hamster IgG completely resolved infections, gamma delta T cell-depleted mice were unable to suppress their infections. Because the number of splenic CD4+ alpha beta T cells in these anti-TCR-gamma delta-treated mice with nonresolving malaria was similar to control mice, it appears that CD4+ alpha beta T cells alone cannot mediate early resolution even though they are known to play a critical role in immunity to blood-stage malaria. Mice treated with anti-CD4 mAb also failed to resolve P. c. adami malaria. Depletion of CD4+ alpha beta T cells from the spleens of infected mice resulted in minimal expansion of the splenic CD4- gamma delta T cell subset compared with infected control mice. Together, these findings indicate that activation of the gamma delta T cell subset, which requires the presence of CD4+ alpha beta T cells, is essential for resolution of acute P. c. adami malaria. To determine whether gamma delta T cells require either Abs or B cells to achieve their protective activity, B cell-deficient JHD mice were treated with the same depleting anti-TCR-gamma delta Abs. Whereas control JHD mice injected with hamster IgG resolved acute P. c. adami malaria, JHD mice depleted of gamma delta T cells failed to do so. We conclude that gamma delta T cells suppress P. c. adami parasitemia by mechanisms of immunity independent of Ab and B cells.
为了确定γδ T细胞对于急性查巴迪疟原虫（P. c. adami）疟疾的清除是否至关重要，我们用仓鼠单克隆抗TCRγδ抗体处理C57BL/6小鼠，以清除γδ T细胞。在接受正常仓鼠IgG的对照小鼠完全清除感染的期间，γδ T细胞耗竭的小鼠无法抑制其感染。由于这些接受抗TCR-γδ处理且疟疾未得到缓解的小鼠脾脏中CD4 + αβ T细胞的数量与对照小鼠相似，因此尽管已知CD4 + αβ T细胞在血液期疟疾免疫中起关键作用，但仅靠它们似乎无法介导早期清除。用抗CD4 mAb处理的小鼠也未能清除P. c. adami疟疾。与感染的对照小鼠相比，从感染小鼠脾脏中清除CD4 + αβ T细胞导致脾脏CD4 - γδ T细胞亚群的扩增最小。这些发现共同表明，需要CD4 + αβ T细胞存在的γδ T细胞亚群的激活对于急性P. c. adami疟疾的清除至关重要。为了确定γδ T细胞是否需要抗体或B细胞来实现其保护活性，用相同的耗竭性抗TCR-γδ抗体处理B细胞缺陷的JHD小鼠。注射仓鼠IgG的对照JHD小鼠能够清除急性P. c. adami疟疾，而γδ T细胞耗竭的JHD小鼠则未能清除。我们得出结论，γδ T细胞通过独立于抗体和B细胞的免疫机制抑制P. c. adami疟原虫血症。
