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首页> 外文期刊>Infection and immunity >Regulation of egg antigen-induced in vitro proliferative response by splenic suppressor T cells in murine Schistosoma japonicum infection.
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Regulation of egg antigen-induced in vitro proliferative response by splenic suppressor T cells in murine Schistosoma japonicum infection.

机译:在小鼠日本血吸虫感染中脾抑制性T细胞调节卵抗原诱导的体外增殖反应。

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Beginning about 5 weeks after infection, C57BL/6J mice infected with Schistosoma japonicum developed granulomas around parasite eggs trapped in the liver. These granulomas attained peak size about 9 weeks after infection and then spontaneously regressed. This regression was also induced by the injection of serum immunoglobulin G1 but not lymphoid cells from chronically infected mice, but it was conceivable that lymphoid cells from mice infected for 10 weeks could also induce regression. We investigated the possibility of cellular suppression of egg antigen-induced immune responses by coculturing spleen cells from 5- to 6-week-infected mice with spleen cells from mice infected for 10 weeks or longer. Mitomycin C-resistant Thy 1.2+, Lyt 2.2+ splenic T cells from mice infected for 10 to 25 weeks consistently suppressed the egg antigen-stimulated proliferation of spleen cells from 5- to 6-week-infected mice. Suppression was dependent upon specific antigen and optimal concentrations of egg antigen and T suppressor cells. Once induced, the suppressor cells were nonspecific. Cultured T cells from uninfected mice also occasionally suppressed the acute spleen cell proliferative response, but these cells were mitomycin C sensitive. These in vitro observations suggest that granulomatous inflammation in vivo may also be down regulated by suppressor T cells and that these cells may also be implicated in the nonspecific depression of cellular and humoral responses to antigens observed during the course of this infection.
机译:感染后约5周开始,感染日本血吸虫的C57BL / 6J小鼠在肝脏中捕获的寄生虫卵周围形成肉芽肿。这些肉芽肿在感染后约9周达到峰值,然后自发消退。通过注射血清免疫球蛋白G1而不是注射来自慢性感染小鼠的淋巴样细胞也可以诱导这种消退,但是可以想象,感染了10周的小鼠的淋巴样细胞也可以引起消退。我们通过将感染5至6周的小鼠的脾细胞与感染小鼠的脾细胞共培养10周或更长时间来研究细胞抑制卵抗原诱导的免疫反应的可能性。来自感染10至25周的小鼠的丝裂霉素C抵抗性Thy 1.2 +,Lyt 2.2+脾脏T细胞始终抑制5-6周感染小鼠的卵抗原刺激的脾细胞增殖。抑制取决于特异性抗原以及卵抗原和T抑制细胞的最佳浓度。诱导后,抑制细胞是非特异性的。来自未感染小鼠的培养T细胞有时也抑制了急性脾细胞的增殖反应,但这些细胞对丝裂霉素C敏感。这些体外观察表明,体内的肉芽肿性炎症也可能被抑制性T细胞下调,并且这些细胞也可能与在感染过程中观察到的对抗原的细胞和体液反应的非特异性抑制有关。

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