A 24000 MW Trypanosoma cruzi antigen is a B-cell activator
A 24000 MW Trypanosoma cruzi antigen is a B-cell activator
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DOI：
10.1046/j.1365-2567.1998.00498.x
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发表时间：
1998-06-01
期刊：
影响因子：
6.4
通讯作者：
Minoprio, P
中科院分区：
文献类型：
--
作者：
DA Silva, AC;Espinoza, AG;Minoprio, P
克氏锥虫是恰加斯病的病原体，是一种感染中美洲和拉丁美洲人类和其他哺乳动物的原生动物寄生虫。已经描述了感染后免疫反应的几种改变，例如细胞和体液反应的严重免疫抑制以及大量多克隆B和t细胞激活，包括自我反应性克隆的扩增。我们研究了腹腔注射重组24 000 MW克氏t病毒特异性抗原（rTc24）对正常和缺陷小鼠免疫应答的影响。我们通过测定CD69激活标记物的表达和脾细胞胸腺嘧啶掺入水平，分析了rTc24在体内和体外的淋巴细胞活化水平和增殖反应。elisa法检测血清中产生抗体的细胞数量，同型特异性酶联免疫吸附法检测血清中免疫球蛋白水平。我们在体内和体外观察到rTc24刺激后脾脏细胞中[H-3]胸腺嘧啶（[H-3]TdR）掺入增加。rTc24诱导的增殖活性与实验所用小鼠品系（包括C3H/HeJ小鼠）无关，排除了rTc24制剂被脂多糖污染的可能性。通过IgM（+）脾细胞上CD69分子表达的增加可以确定，rTc24蛋白的注射优先诱导B细胞的活化。在胸腺型和胸腺型BALB/c小鼠中均发现分泌igm的B细胞显著增加。缺乏B细胞（BALB.Xid）的小鼠对rTc24有反应，但程度较低。这些IgM b细胞数量的增加伴随着注射动物血清中IgM免疫球蛋白水平的升高。我们的结果表明rTc24在b细胞活化中起作用。
Trypanosoma cruzi, the causative agent of Chagas' disease, is a protozoan parasite that infects humans and other mammals in Central and Latin America. Several alterations of the immune response after infection have been described, such as severe immunosuppression of both cellular and humoral responses and massive polyclonal B- and T-cell activation, including the expansion of self-reactive clones. We have investigated the effects of the intraperitoneal injection of a recombinant 24 000 MW T. cruzi-specific antigen (rTc24) on the immune response of normal and deficient strains of mice. We analysed the in vivo and ex vivo levels of lymphocyte activation and the proliferative responses to rTc24 by determining the expression of CD69 activation marker and the levels of thymidine incorporation by spleen cells. The numbers of antibody-producing cells were determined by ELISPOT and the levels of immunoglobulin in the sera by isotype-specific enzyme-linked immunosorbent assay. We observed an increased [H-3]thymidine ([H-3]TdR) incorporation by spleen cells after rTc24 stimulation in vivo and in vitro. This proliferative activity induced by rTc24 was independent of the mouse strain used in the experiments (including C3H/HeJ mice) and ruled out the possibility that rTc24 preparations were contaminated by lipopolysaccharide. The injection of rTc24 protein induced preferentially the activation of B cells, as determined by the increased expression of CD69 molecules on IgM(+) spleen cells. Considerable increases of IgM-secreting B cells were determined in both athymic and euthymic BALB/c mice. Mice that are deficient in B cells (BALB.Xid) responded to rTc24 but to a lesser extent. These increases in IgM B-cell numbers were accompanied by elevated levels of IgM immunoglobulins in the sera of injected animals. Our results suggest a role for rTc24 in B-cell activation.