正常和免疫缺陷小鼠感染疟疾期间未感染红细胞的过早清除。
Premature removal of uninfected erythrocytes during malarial infection of normal and immunodeficient mice.
作者信息
Salmon M G, De Souza J B, Butcher G A, Playfair J H
机构信息
Department of Immunology, UCLMS, London, UK.
出版信息
Clin Exp Immunol. 1997 Jun;108(3):471-6. doi: 10.1046/j.1365-2249.1997.3991297.x.
Anaemia during blood-stage plasmodial infections is known to be due to at least three mechanisms: direct destruction of erythrocytes by the intra-erythrocytic parasite, inhibition of erythropoiesis, and premature removal of uninfected erythrocytes. The removal of the uninfected erythrocytes is considered by many to be dependent on an antibody-mediated mechanism. Our investigations involving normal, severe combined immunodeficient (SCID) and nude BALB/c mice and the murine malaria parasite Plasmodium yoelii, indicate that this mechanism is unlikely. The process of removal of uninfected erythrocytes was reduced in SCID mice but could not be enhanced by the passive transfer of serum from infected immunocompetent mice. Macrophage activation, as judged by the removal of xenogeneic erythrocytes, did not differ in the three strains of mice. Changes in the erythrocytes themselves may be responsible for their shortened lifespan.
已知血液阶段疟原虫感染期间的贫血至少由三种机制引起
红细胞内寄生虫对红细胞的直接破坏、红细胞生成的抑制以及未感染红细胞的过早清除。许多人认为未感染红细胞的清除依赖于抗体介导的机制。我们涉及正常、严重联合免疫缺陷（SCID）和裸BALB/c小鼠以及鼠疟原虫约氏疟原虫的研究表明，这种机制不太可能。SCID小鼠中未感染红细胞的清除过程有所减少，但从感染的免疫 competent 小鼠被动转移血清并不能增强这一过程。通过异种红细胞的清除来判断，巨噬细胞激活在这三种小鼠品系中并无差异。红细胞自身的变化可能导致其寿命缩短。
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