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红细胞凝集:疟原虫感染红细胞的一种新的细胞黏附特性。

Rosetting: a new cytoadherence property of malaria-infected erythrocytes.

作者信息

David P H, Handunnetti S M, Leech J H, Gamage P, Mendis K N

机构信息

Unite d' Immunoparasitologie, Institut Pasteur, Paris, France.

出版信息

Am J Trop Med Hyg. 1988 Mar;38(2):289-97. doi: 10.4269/ajtmh.1988.38.289.

Abstract

Plasmodium fragile infection of the toque monkey is a natural host-parasite association in which parasite sequestration occurs as during P. falciparum infection of humans. We have studied parasite sequestration of P. fragile and demonstrated the existence of a new property of cytoadherence of infected erythrocytes, "rosetting," which is defined as the agglutination of uninfected erythrocytes around parasitized erythrocytes. Rosetting in vitro and sequestration in vivo appear simultaneously as the parasite matures. The spleen plays a role in modulating cytoadherence; both sequestration and rosetting, which occur with cloned parasites from spleen-intact animals, are markedly reduced in splenectomized animals infected with parasites derived from the same clone. Sequestration and rosetting can be reversed by immune serum. Protease treatment of infected blood abolishes rosetting; however, if treatment is performed at an early stage of schizogony, rosetting reappears if parasites are allowed to further develop in the absence of protease. These results indicate that with P. fragile in its natural primate host, rosetting and sequestration are related to the presence on the infected erythrocyte surface of a parasite-derived antigenic component, the expression of which is modulated by the spleen.

摘要

脆弱疟原虫感染帽猴是一种自然宿主 - 寄生虫关联,其中寄生虫滞留现象与人类感染恶性疟原虫时一样会发生。我们研究了脆弱疟原虫的寄生虫滞留现象,并证明了受感染红细胞存在一种新的细胞黏附特性,即“花结形成”,它被定义为未感染红细胞在被寄生红细胞周围的凝集。随着寄生虫成熟,体外花结形成和体内滞留现象同时出现。脾脏在调节细胞黏附方面发挥作用;来自脾脏完整动物的克隆寄生虫所发生的滞留和花结形成,在感染相同克隆寄生虫的脾切除动物中明显减少。滞留和花结形成可被免疫血清逆转。用蛋白酶处理感染血液可消除花结形成;然而,如果在裂殖生殖早期进行处理,在没有蛋白酶的情况下让寄生虫进一步发育,花结形成会再次出现。这些结果表明,在其天然灵长类宿主中,脆弱疟原虫的花结形成和滞留与受感染红细胞表面存在寄生虫衍生的抗原成分有关,其表达受脾脏调节。

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