Coutelier Jean-Paul, Detalle Laurent, Musaji Andrei, Meite Mory, Izui Shozo
The Unit of Experimental Medicine, Université catholique de Louvain, Brussels, Belgium.
Ann N Y Acad Sci. 2007 Aug;1109:151-7. doi: 10.1196/annals.1398.018.
Viruses are associated with the development of autoantibody-mediated blood autoimmune diseases. A two-step mechanism could explain virus involvement in the development of experimental hemolytic anemia. Immunization of normal mice with rat erythrocytes results in an autoantibody production that could be enhanced by viral infection, without erythrocyte destruction. Inoculation of the same virus when autoantibodies are at high levels triggers clinical anemia. This results from macrophage activation by gamma-interferon, leading to exacerbated erythrophagocytosis. Thus the development of anemia during the course of viral infection may require two independent stimuli, in which the first triggers autoantibody production and the second enhances the pathogenicity of these autoantibodies.
病毒与自身抗体介导的血液自身免疫性疾病的发生有关。一种两步机制可以解释病毒在实验性溶血性贫血发生过程中的作用。用大鼠红细胞对正常小鼠进行免疫会产生自身抗体,病毒感染可增强这种自身抗体的产生,而不会导致红细胞破坏。当自身抗体水平较高时接种同一种病毒会引发临床贫血。这是由γ干扰素激活巨噬细胞导致红细胞吞噬加剧所致。因此,病毒感染过程中贫血的发生可能需要两个独立的刺激因素,其中第一个刺激因素触发自身抗体的产生,第二个刺激因素增强这些自身抗体的致病性。