Wunderlich F, Benten W P, Bettenhaeuser U, Schmitt-Wrede H P, Mossmann H
Division of Parasitology, Heinrich-Heine-University, Duesseldorf, FRG.
Parasite Immunol. 1992 May;14(3):307-20. doi: 10.1111/j.1365-3024.1992.tb00470.x.
Testosterone (Te) is known to suppress immunity and to increase host susceptibility to many parasites. This study investigates the action of Te on immunity acquired against blood-stages of the malaria parasite Plasmodium chabaudi in female mice of the inbred strain C57BL/10. Our data show: (i) About 90% of mice infected with 10(6) P. chabaudi-infected erythrocytes are able to develop protective immune mechanisms which become evident in self-healing the infection. The capability of self-healing is lost when mice are pretreated with Te for 3 weeks. (ii) Mice which have self-healed infections acquire immunity to homologous rechallenge. Concomitantly, mice become Te-unresponsive in that their acquired immunity is not suppressible by Te-treatment. (iii) Flow cytometry reveals that Te-pretreatment entails an increase of CD8+ cells and a decrease of Ig+ cells by about 4% in spleens of non-immune mice. In immune mice, however, there is a Te-unresponsiveness of the percental distribution of splenic cell populations. (iv) Adoptive transfer experiments indicate that immunity is conferred by spleen cells, presumably non-T-cells. These cells are Te-unresponsive, since they exert their effect in Te-pretreated mice in the presence of Te. (v) Te-unresponsive immunity can be also transferred by serum, especially the IgG-fraction, obtained from immune mice. Our data demonstrate that Te prevents the development of protective immunity against P. chabaudi infections. However, when once established, protective immunity becomes unresponsive to Te. Our data suggest that the effector mechanisms of protective immunity involve Te-unresponsive B cells secreting protective IgG-antibodies.
已知睾酮（Te）会抑制免疫力，并增加宿主对许多寄生虫的易感性。本研究调查了Te对近交系C57BL/10雌性小鼠针对疟原虫查巴迪疟原虫血液阶段所获得免疫力的作用。我们的数据显示：（i）约90%感染10⁶个感染查巴迪疟原虫红细胞的小鼠能够形成保护性免疫机制，这在感染自愈中变得明显。当小鼠用Te预处理3周时，自愈能力丧失。（ii）自愈感染的小鼠获得了对同源再次攻击的免疫力。与此同时，小鼠对Te无反应，因为它们获得的免疫力不能被Te治疗所抑制。（iii）流式细胞术显示，Te预处理使非免疫小鼠脾脏中的CD8⁺细胞增加，Ig⁺细胞减少约4%。然而，在免疫小鼠中，脾细胞群体的百分比分布对Te无反应。（iv）过继转移实验表明，免疫力由脾细胞赋予，可能是非T细胞。这些细胞对Te无反应，因为它们在存在Te的情况下在Te预处理的小鼠中发挥作用。（v）对Te无反应的免疫力也可以通过从免疫小鼠获得的血清，特别是IgG部分来转移。我们的数据表明，Te会阻止针对查巴迪疟原虫感染的保护性免疫的发展。然而，一旦建立，保护性免疫对Te就无反应。我们的数据表明，保护性免疫的效应机制涉及分泌保护性IgG抗体的对Te无反应的B细胞。
