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疟疾导致人类、猴子和小鼠脾脏γδ T细胞增加。

Malaria-induced increase of splenic gamma delta T cells in humans, monkeys, and mice.

作者信息

Nakazawa S, Brown A E, Maeno Y, Smith C D, Aikawa M

机构信息

Institute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106.

出版信息

Exp Parasitol. 1994 Nov;79(3):391-8. doi: 10.1006/expr.1994.1101.

Abstract

The number and distribution of gamma delta T cells in spleens from patients who died of cerebral malaria and from rhesus monkeys severely infected with Plasmodium coatneyi were examined by immunocytochemistry. gamma delta T cells were significantly increased in these spleens. In a rodent malaria model using Plasmodium chabaudi adami, an avirulent strain of murine malaria parasites, the degree of parasitemia appears to be modulated by the number of gamma delta T cells in the spleen. As parasitemia increases, these T cells increase in number. At some critical point, gamma delta T cells in collaboration with macrophages and alpha beta T cells apparently start to clear parasitized erythrocytes from the blood, leading to an abatement of the parasitemia, which is followed by a reduction in the number of gamma delta T cells. This gamma delta T cell phenomenon may be responsible for the self-limiting infection in mice.

摘要

通过免疫细胞化学方法,对死于脑型疟疾的患者以及严重感染科氏疟原虫的恒河猴脾脏中γδ T细胞的数量和分布进行了检测。这些脾脏中的γδ T细胞显著增加。在使用无毒力的鼠疟原虫查巴迪疟原虫的啮齿动物疟疾模型中,疟原虫血症的程度似乎受到脾脏中γδ T细胞数量的调节。随着疟原虫血症增加,这些T细胞数量增多。在某个关键点上,γδ T细胞与巨噬细胞和αβ T细胞协同作用,显然开始从血液中清除被寄生的红细胞,导致疟原虫血症减轻,随后γδ T细胞数量减少。这种γδ T细胞现象可能是小鼠感染自我限制的原因。

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