Vincendeau P, Daëron M, Daulouede S
Infect Immun. 1986 Sep;53(3):600-5. doi: 10.1128/iai.53.3.600-605.1986.
The phagocytosis of Trypanosoma musculi by macrophages in the presence of specific antibodies was investigated. In 14-day-infected mice, opsonic antibodies were detected in serum, and phagocytosis of parasites by peritoneal macrophages was observed. The mechanism of T. musculi phagocytosis was analyzed. The binding of trypanosomes to peritoneal macrophages and J774 cells was observed in the presence of serum from hyperimmune mice and from mice infected 14 or 28 days earlier, but not in the presence of control mouse serum or sera from 7-day-infected mice. Binding was partially inhibited by mouse monoclonal immunoglobulins G1 (IgG1) or IgG2a and almost completely inhibited by a mixture of both. Binding was also partially inhibited by the anti-Fc gamma 1/gamma 2b receptor monoclonal antibody 2.4G2. Binding of T. musculi was also induced by fractions of serum from 28-day-infected mice obtained by protein A-Sepharose chromatography. Only the IgG1-rich fraction eluted at pH 6.0 and the IgG2a-rich fraction eluted at pH 4.5 promoted binding which could be almost completely inhibited by monoclonal IgG1 and IgG2a. These data indicate that IgG1 and IgG2a anti-T. musculi antibodies are responsible for the phagocytosis of T. musculi by mouse macrophages and both Fc gamma 2a and Fc gamma 1/gamma 2b receptors are involved. Such a mechanism is likely to account for the elimination of parasites in T. musculi-infected mice.
研究了在特异性抗体存在的情况下巨噬细胞对鼠锥虫的吞噬作用。在感染14天的小鼠血清中检测到调理素抗体,并观察到腹膜巨噬细胞对寄生虫的吞噬作用。分析了鼠锥虫的吞噬机制。在超免疫小鼠以及感染14天或28天的小鼠血清存在的情况下,观察到锥虫与腹膜巨噬细胞和J774细胞的结合,但在对照小鼠血清或感染7天的小鼠血清存在的情况下未观察到结合。结合作用被小鼠单克隆免疫球蛋白G1(IgG1)或IgG2a部分抑制,而被两者的混合物几乎完全抑制。结合作用也被抗Fcγ1/γ2b受体单克隆抗体2.4G2部分抑制。鼠锥虫的结合也由通过蛋白A-琼脂糖凝胶层析从感染28天的小鼠血清中获得的组分诱导。仅在pH 6.0洗脱的富含IgG1的组分和在pH 4.5洗脱的富含IgG2a的组分促进结合,这几乎可被单克隆IgG1和IgG2a完全抑制。这些数据表明,IgG1和IgG2a抗鼠锥虫抗体负责小鼠巨噬细胞对鼠锥虫的吞噬作用,并且Fcγ2a和Fcγ1/γ2b受体均参与其中。这样一种机制可能解释了鼠锥虫感染小鼠中寄生虫的清除。