Davis J K, Cassell G H, Minion F C, Wise K S
Isr J Med Sci. 1981 Jul;17(7):633-6.
Many pathogenic mycoplasmas induce chronic inflammation as a consequence of their ability of circumvent or block immunological attack. This may be due to the organisms's intrinsic properties or to factors that arise from mycoplasma host-cell interactions. Based upon present evidence, the most likely mechanisms are antibody and/or phagocyte inefficiency, alteration of lymphocyte responsiveness due to the nonspecific mitogenicity of mycoplasmas, and antigenic disguise via acquisition of host antigens. The latter is not only an important mechanism by which the organisms could evade or alter the host immunological response, but one which may serve as a stimulus for autoimmune reactions.
许多致病性支原体能够规避或阻断免疫攻击，从而引发慢性炎症。这可能是由于支原体本身的特性，或者是支原体与宿主细胞相互作用产生的因素所致。根据目前的证据，最可能的机制是抗体和/或吞噬细胞功能低下、支原体的非特异性促有丝分裂活性导致淋巴细胞反应性改变，以及通过获取宿主抗原进行抗原伪装。后者不仅是支原体逃避或改变宿主免疫反应的重要机制，而且可能是自身免疫反应的刺激因素。
