Lambre C R, Thibon M, Le Maho S, Di Bella G
Immunology. 1983 Jun;49(2):311-9.
Guinea-pig erythrocytes that had been exposed to influenza A virus or Vibrio cholerae neuraminidase activated the classical complement pathway in autologous serum. Because all viral particles were eluted from the treated cells, activation was not dependent on anti-viral antibodies or on the particles themselves. After a threshold of 45-55% desialation, had been reached, the relative capacity of treated cells to activate complement increased very rapidly with desialation. Desialation unmasked sites on which natural auto-antibodies of the IgM class were fixed. Antibody fixation on the membrane led to C3b deposition on the cell membrane and activation of the classical complement sequence then cell lysis. The relevance of in vitro lysis of desialated cells to in vivo clearance of these cells is not certain because C4-deficient guinea-pigs were able to eliminate desialated cells from the blood stream as efficiently as did normal guinea-pigs. Nevertheless, membrane desialation occurring during myxovirus infection could lead to autoimmunity and tissue changes, as well as to recovery by eliminating virus-modified cells.
暴露于甲型流感病毒或霍乱弧菌神经氨酸酶的豚鼠红细胞，可在自体血清中激活经典补体途径。由于所有病毒颗粒都从处理过的细胞上洗脱下来，因此激活不依赖于抗病毒抗体或颗粒本身。在达到45%-55%的去唾液酸化阈值后，处理过的细胞激活补体的相对能力会随着去唾液酸化而迅速增加。去唾液酸化会暴露出IgM类天然自身抗体固定的位点。抗体在细胞膜上的固定导致C3b沉积在细胞膜上，并激活经典补体序列，进而导致细胞裂解。去唾液酸化细胞的体外裂解与这些细胞在体内清除的相关性尚不确定，因为C4缺陷型豚鼠能够与正常豚鼠一样有效地从血流中清除去唾液酸化细胞。然而，黏液病毒感染期间发生的细胞膜去唾液酸化可能导致自身免疫和组织变化，以及通过清除病毒修饰的细胞实现恢复。
