Langhorne J, Mombaerts P, Tonegawa S
Max-Planck-Institut für Immunbiologie, Freiburg, Germany.
Int Immunol. 1995 Jun;7(6):1005-11. doi: 10.1093/intimm/7.6.1005.
Mice lacking T cells with alpha beta TCR (TCR beta-/-) or gamma delta TCR (TCR delta-/-) were infected with the erythrocytic stages of the malaria parasite, Plasmodium chabaudi chabaudi (AS). Mice without gamma delta T cells could control and reduce a primary infection of P. chabaudi with a slight delay in the time of clearance of the acute phase of infection and significantly higher recrudescent parasitaemias compared with control intact mice. TCR delta -/- mice had higher levels of both serum Ig and malaria-specific antibodies of the isotypes IgG3 and IgG1 compared with control mice. TCR beta -/- mice, despite a striking increase in NK1.1+ cells and the presence of gamma delta T cells, were unable to clear their infection. Although the plasma of TCR beta -/- mice contained all Ig isotypes before and during a primary infection, they were unable to produce significant levels of malaria-specific IgG antibodies, suggesting that in the absence of alpha beta T cells gamma delta T cells are not able to provide efficient help for antibody production.
缺乏αβT细胞受体(TCRβ-/-)或γδT细胞受体(TCRδ-/-)的小鼠感染了疟原虫恰氏疟原虫(AS)的红细胞期。缺乏γδT细胞的小鼠能够控制并减轻恰氏疟原虫的初次感染,不过在清除感染急性期的时间上稍有延迟,且与对照的正常小鼠相比,复发时的疟原虫血症显著更高。与对照小鼠相比,TCRδ-/-小鼠的血清Ig以及IgG3和IgG1等亚型的疟疾特异性抗体水平都更高。TCRβ-/-小鼠尽管NK1.1+细胞显著增加且存在γδT细胞,却无法清除感染。虽然TCRβ-/-小鼠的血浆在初次感染前和感染期间含有所有Ig亚型,但它们无法产生显著水平的疟疾特异性IgG抗体,这表明在缺乏αβT细胞的情况下,γδT细胞无法为抗体产生提供有效的帮助。