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

小鼠感染了约氏疟原虫，这是一种血液期寄生虫。在感染后第7天，肝和脾均为炎症部位。肝和脾中的主要扩增细胞为NK1.1中间αβTcr(αβTcr)，但NK1.1+αβTcr的数量不变或略有增加。这些TCR^&lt；int&gt；细胞起源于胸腺外，或由另一种胸腺内途径产生，与传统的胸腺起源的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。从约氏疟原虫感染后恢复的小鼠肝脏中纯化的TCR^&lt；int&gt；细胞被转移到6.5Gy射线照射的小鼠体内，可以保护小鼠免受疟疾的侵袭。有趣的是，在恢复后，对疟疾的免疫力似乎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^&lt；int&gt；细胞与预防疟疾感染密切相关，因此，一年前从疟疾中恢复的小鼠失去了这种免疫。

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.