Abstract
The mode and degree of tissue specific immunocytolysis closely depend on the nature of cell-surface antigens and on the competition or balance of humoral and cell-mediated immunity. The modification of cell surface membrane by neuraminidase-treatment induced the higher susceptibility to complement-dependent cytolysis, probably on account of exposure of cryptic sites or aggregation (clustering) of sites which may be tissue specific and/or histocompatibility antigen determinants. Under the existence of large amount of antisera, complement-dependent cytolysis was dominant. On the contrary, under the situation of low dose anti-sera, normal adherent-cell-mediated cytolysis was more effective. This kind of cytolysis was inhibited easily by serum factor(s), which could be IgG, and block Fc receptor of adherent cells in competition with anti-Ig14. Although the role of serum-factor(s) is still unknown, it may act an important role in the process of establishment of autoimmune diseases.
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