Lelchuk R, Sprott V M, Playfair J H
Clin Exp Immunol. 1981 Aug;45(2):433-8.
The suppression of the contact sensitivity of oxazolone in murine malaria is shown to be mediated by non-specific T suppressor cells, but to a different extent in infection caused by two different species of parasite. Depletion of T suppressor cells in vivo and/or anti-Thy 1.2 treatment in vitro indicated that in mice infected with P. berghei the suppressor effect was largely mediated by T cells. By contrast, in mice infected with a lethal strain of P. yoelii it was only partly due to T cells; B suppressor cells and/or macrophages may also be involved. However, depletion of T suppressor cells in vivo had no effect on the course of the parasitaemia or on the survival time. Therefore, we postulate that this kind of non-specific immunosuppression cannot be regarded as a major cause of lethality.
已表明,小鼠疟疾中恶唑酮接触敏感性的抑制是由非特异性T抑制细胞介导的,但在由两种不同寄生虫物种引起的感染中,其程度有所不同。体内T抑制细胞的耗竭和/或体外抗Thy 1.2处理表明,在感染伯氏疟原虫的小鼠中,抑制作用主要由T细胞介导。相比之下,在感染约氏疟原虫致死株的小鼠中,这仅部分归因于T细胞;B抑制细胞和/或巨噬细胞也可能参与其中。然而,体内T抑制细胞的耗竭对寄生虫血症的进程或存活时间没有影响。因此,我们推测这种非特异性免疫抑制不能被视为致死的主要原因。