Washburn L R, Ramsey J R
Department of Microbiology, University of South Dakota, Vermillion 57069.
Isr J Med Sci. 1987 May;23(5):434-8.
LEW rats experimentally infected with Mycoplasma arthritidis failed to express metabolism inhibition (MI) antibodies. Our hypothesis was that rats failed to immunologically recognize the antigens responsible for eliciting those antibodies. LEW rats, injected i.v. with M. arthritidis, recognized only two low-MW surface antigens by radioimmunoprecipitation by 1 week after injection. However, by 6 weeks these rats recognized most of the same M. arthritidis surface antigens by Western blot and radioimmunoprecipitation as were recognized by immunized rabbits. The most important exception was a 47-to 50-kDa (kilodalton) surface protein that was antigenic only for rabbits. We had previously produced two monoclonal antibodies with MI activity that recognized two distinct M. arthritidis epitopes. However, neither of these corresponded to the antigen that rats failed to recognize, and LEW rats produced IgG antibodies against both monoclonal antibody-defined "MI antigens." Therefore, the failure of rats to express MI activity against M. arthritidis remains unexplained.
实验感染关节炎支原体的LEW大鼠未能表达代谢抑制（MI）抗体。我们的假设是，大鼠未能在免疫上识别引发这些抗体的抗原。静脉注射关节炎支原体的LEW大鼠在注射后1周通过放射免疫沉淀仅识别出两种低分子量表面抗原。然而，到6周时，这些大鼠通过蛋白质印迹和放射免疫沉淀识别出的大多数关节炎支原体表面抗原与免疫兔所识别的相同。最重要的例外是一种47至50千道尔顿的表面蛋白，它仅对兔具有抗原性。我们之前制备了两种具有MI活性的单克隆抗体，它们识别两种不同的关节炎支原体表位。然而，这两种抗体都与大鼠未能识别的抗原不对应，并且LEW大鼠产生了针对两种单克隆抗体定义的“MI抗原”的IgG抗体。因此，大鼠未能表达针对关节炎支原体的MI活性的原因仍无法解释。
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