Hernández-Munaín C, De Diego J L, Bonay P, Gironés N, Fresno M
Centro de Biología Molecular, Universidad Autónoma de Madrid, Spain.
Biol Res. 1993;26(1-2):209-18.
Chagas' disease results from the infection of the protozoan parasite Trypanosoma cruzi and affects several million people in South America. Several alterations of the immune response have been described in this disease, such as severe immunosuppression of both cellular and humoral responses and the induction of autoantibodies crossreacting with host cells and tissues. We described here a GPI-linked 50/55 kDa antigen (GP50/55) present on the T. cruzi membrane, but not in the membrane of other parasites of the family Trypanosomatidae. We have obtained several monoclonal antibodies which specifically recognize this molecule. One of these GP50/55-specific mAbs (C10) crossreacts with a 28 kDa antigen expressed on the membrane of activated mouse and human T and B lymphocytes, after "in vitro" activation with mitogens, phorbol esters, or antigen, and on several murine T and B lymphocyte cell lines. Furthermore, this mAb was able to suppress mouse and human T and B cell proliferation to any of those stimuli. In addition, sera from T. cruzi-infected mice or Chagasic patients but not from uninfected mice or control patients contain antibodies which recognize a similar p28 antigen and also suppress the proliferation of human T lymphocytes. These results suggest a possible role of autoantibodies as an alternative mechanism for T. cruzi-associated immunosuppression.
恰加斯病由原生动物寄生虫克氏锥虫感染引起，影响南美洲数百万人。该病已被描述出多种免疫反应改变，如细胞免疫和体液免疫的严重免疫抑制以及诱导与宿主细胞和组织发生交叉反应的自身抗体。我们在此描述了一种存在于克氏锥虫膜上但不存在于锥虫科其他寄生虫膜上的糖基磷脂酰肌醇（GPI）连接的50/55 kDa抗原（GP50/55）。我们获得了几种特异性识别该分子的单克隆抗体。其中一种GP50/55特异性单克隆抗体（C10）与经丝裂原、佛波酯或抗原“体外”激活后的活化小鼠和人T及B淋巴细胞膜上表达的28 kDa抗原发生交叉反应，也与几种小鼠T和B淋巴细胞系发生交叉反应。此外，该单克隆抗体能够抑制小鼠和人T及B细胞对任何这些刺激的增殖。另外，来自克氏锥虫感染小鼠或恰加斯病患者的血清（而非未感染小鼠或对照患者的血清）含有识别类似p28抗原的抗体，并且也能抑制人T淋巴细胞的增殖。这些结果提示自身抗体可能作为克氏锥虫相关免疫抑制的一种替代机制发挥作用。
