Targets as the malarial infection and the attack of extrathymic T cells : MHC^+ erytherocytes in the bone marrow

小鼠感染疟原虫（P.）约氏血阶段寄生虫在疟疾感染的第7天开始时，肝脏和脾脏都是炎症的部位。在肝脏和脾脏中发现主要的扩增细胞是NK 1.1中间αβTCR（αβTCR^<int>），尽管NK 1.1 ^+αβTCR^细胞的数量<int>保持不变或略有增加。这些TCR γ<int>细胞是胸腺外来源的或通过替代性胸腺内途径产生，并且与胸腺来源的常规T细胞不同。在疟疾感染期间，常规T细胞的数量根本没有增加。从<int>约氏疟原虫感染恢复的小鼠的肝脏中纯化的TCR γ细胞在转移到6.5 Gy照射的小鼠中时保护小鼠免受疟疾。有趣的是，对疟疾的免疫力似乎在恢复后随着时间的推移而消失。也就是说，一年前从疟疾中恢复的小鼠再次变得容易感染疟疾。目前的结果表明，TCR γ<int>细胞与抗疟疾感染的保护密切相关，因此，一年前从疟疾中恢复的小鼠失去了这种免疫力。

Mice were infected with Plasmodium(P.)yoelii, blood-stage parasites. Both the liver and spleen were the sites of inflammation during malarial infection at the beginning of day 7. The major expanding cells were found to be NK1.1 intermediate αβTCR(αβTCR^<int>)in the liver and spleen, although the population of NK1.1^+αβTCR^<int> cells remained constant or slightly increased. These TCR^<int> cells are of extrathymic origin or are generated by an alternative intrathymic pathway, and are distinguished from conventional T cells of thymic origin. During malarial infection, the population of conventional T cells did not increase at all. TCR^<int> cells purified from the liver of mice which had recovered from P.yoelii infection protected mice from malaria when they were transferred into 6.5 Gy-irradiated mice. Interestingly, the immunity against malaria seemed to disappear as a function of time after the recovery. Namely, mice which had recovered from malaria one year previously again became susceptible to malarial infection. The present results suggest that TCR^<int> cells are intimately associated with the protection against malarial infection and, therefore, that the mice which had recovered from malaria one year previously lost such immunity.