Pancré V, Schellekens H, Van der Meide P, Vorng H, Delanoye A, Capron A, Auriault C
Centre d'Immunologie et de Biologie Parasitaire, INSERM 167, Lille, France.
Cell Immunol. 1990 Jan;125(1):58-64. doi: 10.1016/0008-8749(90)90062-v.
We demonstrate here that a second mechanism of platelet activation dependent on lymphokine could also take place in the expression of platelet cytotoxicity against Schistosoma mansoni in vitro. Indeed, IgE, as previously described, but also IFN-gamma, present in the sera of infected rats, together induce platelets from normal rats into cytotoxic effectors for the parasitic larvae. This second mechanism appears also effective in vivo since the passive transfer of normal platelets treated by recombinant IFN-gamma (rIFN-gamma) and the administration of rIFN-gamma to rats conferred a protective immunity to S. mansoni.
我们在此证明，在体外针对曼氏血吸虫的血小板细胞毒性表达中，还可能发生一种依赖淋巴因子的血小板激活的第二种机制。实际上，如先前所述，感染大鼠血清中的IgE以及IFN-γ共同诱导正常大鼠的血小板成为寄生幼虫的细胞毒性效应物。这种第二种机制在体内似乎也有效，因为用重组IFN-γ（rIFN-γ）处理的正常血小板的被动转移以及向大鼠施用rIFN-γ赋予了对曼氏血吸虫的保护性免疫。
