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首页> 外文期刊>Infection and immunity >Infection with Trypanosoma cruzi selectively upregulates B7-2 molecules on macrophages and enhances their costimulatory activity.
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Infection with Trypanosoma cruzi selectively upregulates B7-2 molecules on macrophages and enhances their costimulatory activity.

机译：克氏锥虫感染可选择性上调巨噬细胞上的B7-2分子并增强其共刺激活性。

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T-cell-mediated immune responses are essential for protection against infection with the protozoan Trypanosoma cruzi. In this study, we investigated the influence of infection of murine macrophages with T. cruzi on costimulatory signals for T lymphocytes provided by these cells. We demonstrate that bone marrow-derived macrophages (BMMph) selectively and strongly upregulate expression of B7-2 molecules after infection, while the expression of other costimulatory molecules such as B7-1, intercellular adhesion molecule 1, lymphocyte function-associated antigen 3, and heat-stable antigen is not significantly affected. Infection by live trypanosomes was required. As a consequence of the strong B7-2 upregulation, the infected macrophages are able to induce proliferation of splenic CD4+ T cells in the presence of anti-CD3 antibodies with much higher efficiency than uninfected macrophages. Costimulation could be inhibited by an antibody to B7-2. Furthermore, costimulatory activity for established T-cell clones of Th1 and Th2 phenotype was also strongly enhanced in BMMph by infection with T. cruzi. Th1 cells stimulated either via anti-CD3 antibodies or via specific antigen proliferated with higher efficiency in the presence of infected macrophages than in the presence of uninfected cells. BMMph stimulated with gamma interferon (IFN-gamma), expressing elevated levels of B7-2 molecules, are also able to enhance Th1 cell proliferation, which was highest, using macrophages which were infected and in parallel were stimulated with IFN-gamma. Noteworthy, for cloned Th2 cells, the mechanism of costimulation differed, because costimulation of Th2 cells was not dependent on B7-2 upregulation but was due to secretion of interleukin-1alpha. These findings demonstrate that infection of macrophages with T. cruzi transforms the macrophage into a potent costimulatory cell based on the induction of two different costimulatory activities.
机译：T细胞介导的免疫反应对于防止原生动物克氏锥虫感染至关重要。在这项研究中，我们调查了鼠巨噬细胞感染克氏锥虫对这些细胞提供的T淋巴细胞共刺激信号的影响。我们证明骨髓源性巨噬细胞（BMMph）有选择地并强烈上调感染后的B7-2分子表达，而其他共刺激分子如B7-1，细胞间粘附分子1，淋巴细胞功能相关抗原3和热稳定抗原没有受到明显影响。需要通过活锥虫感染。由于强烈的B7-2上调，在存在抗CD3抗体的情况下，被感染的巨噬细胞能够诱导脾CD4 + T细胞的增殖，其效率要比未感染的巨噬细胞高得多。共刺激可被抗B7-2的抗体抑制。此外，通过感染克氏锥虫，BMMph中对已建立的Th1和Th2表型T细胞克隆的共刺激活性也大大增强。在存在感染的巨噬细胞的情况下，通过抗CD3抗体或通过特异性抗原刺激的Th1细胞的增殖效率要高于未感染细胞的增殖效率。表达高水平的B7-2分子的γ干扰素（IFN-γ）刺激的B​​MMph也能够增强巨噬细胞，被感染并平行地用IFN-γ刺激，从而提高了Th1细胞的增殖，这是最高的。值得注意的是，对于克隆的Th2细胞，共刺激的机制有所不同，因为Th2细胞的共刺激不依赖于B7-2上调，而是由于白介素-1α的分泌。这些发现表明，基于两种不同的共刺激活性的诱导，用克氏锥虫感染巨噬细胞将巨噬细胞转化为有效的共刺激细胞。

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