Lelchuk R, Playfair J H
Clin Exp Immunol. 1980 Dec;42(3):428-35.
A comparative study of non-specific immunosuppression by malaria has been carried out in five situations: in both unvaccinated and vaccinated mice infected with the lethal Plasmodium yoelii or the lethal Plasmodium berghei, and in the unvaccinated non-lethal P. yoelii infection. Spleen cells showed a suppressive effect on the normal blastogenic response to mitogens. This suppression was strongest in the mice vaccinated before infection with the lethal P. yoelii and in those infected with non-lethal P. yoelii, suggesting that the suppressive effect did not interfere with recovery. Silica, anti-Thy-1, and indomethacin treatment suggested that this suppression was caused by macrophages. However, the plaque-forming cell response to sheep RBC in vivo was suppressed equally in every case at the peak of the parasitaemia, whereas the suppression of contact sensitivity to oxazolone was strongest in mice with fatal infections. We suggest that different suppressor mechanisms operate in malaria, some being harmful to the host and others possibly beneficial.
在感染致死性约氏疟原虫或伯氏疟原虫的未接种疫苗和接种疫苗的小鼠中，以及在未接种疫苗的非致死性约氏疟原虫感染中。脾细胞对丝裂原的正常增殖反应表现出抑制作用。这种抑制在感染致死性约氏疟原虫前接种疫苗的小鼠和感染非致死性约氏疟原虫的小鼠中最为强烈，表明这种抑制作用不会干扰恢复。二氧化硅、抗Thy-1和吲哚美辛处理表明这种抑制是由巨噬细胞引起的。然而，在寄生虫血症高峰期，每种情况下对绵羊红细胞的体内空斑形成细胞反应均受到同等程度的抑制，而对恶唑酮的接触敏感性抑制在致命感染小鼠中最为强烈。我们认为，疟疾中存在不同的抑制机制，有些对宿主有害，而有些可能有益。
