Webster A D, Furr P M, Hughes-Jones N C, Gorick B D, Taylor-Robinson D
Division of Immunological Medicine, Clinical Research Centre, Harrow, Middlesex, UK.
Clin Exp Immunol. 1988 Mar;71(3):383-7.
We have shown that mycoplasmas bind spontaneously to neutrophils, as well as directly activating the first component of complement with probable subsequent binding through neutrophil complement receptors. Thus, antibody is not required to opsonize mycoplasmas for neutrophil phagocytosis. Furthermore, mycoplasmas remain viable when phagocytosed in the absence of antibody and may be carried inside neutrophils to various parts of the body to cause infection (e.g. joints). We found that antibody alone inhibits the growth of mycoplasmas in vitro. These observations suggest that the role of antibodies is to control the growth of mycoplasmas on mucosal surfaces; neutrophils play no part in defence and may even aid dissemination of the infection. This helps to explain why patients with hypogammaglobulinaemia are prone to systemic mycoplasma infections.
我们已经表明,支原体可自发结合至中性粒细胞,同时直接激活补体的第一成分,随后可能通过中性粒细胞补体受体发生结合。因此,在中性粒细胞吞噬支原体的过程中,无需抗体进行调理。此外,在无抗体存在的情况下被吞噬时,支原体仍可存活,并可能被携带至中性粒细胞内,输送至身体各个部位从而引发感染(如关节)。我们发现,单独的抗体可在体外抑制支原体生长。这些观察结果表明,抗体的作用是控制支原体在黏膜表面的生长;中性粒细胞在防御过程中不起作用,甚至可能有助于感染的传播。这有助于解释为什么低丙种球蛋白血症患者易患全身性支原体感染。