Mesenteric lymph node T cells but not splenic T cells maintain their proliferative response to concanavalin-A following peroral infection with Toxoplasma gondii.
Mesenteric lymph node T cells but not splenic T cells maintain their proliferative response to concanavalin-A following peroral infection with Toxoplasma gondii.
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经口弓形虫感染后，肠系膜淋巴结 T 细胞（而非脾 T 细胞）维持对刀豆球蛋白 A 的增殖反应。
DOI：
10.1046/j.1365-3024.1998.00162.x
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发表时间：
1998
影响因子：
2.2
通讯作者：
Suzuki,Y
中科院分区：
文献类型：
--
作者：
Neyer,LE;Kang,H;Remington,JS;Suzuki,Y
小鼠感染弓形虫后对T细胞反应性的抑制已被广泛应用于脾细胞的研究。因为感染的自然途径是。在经口感染弓形虫的小鼠中，我们观察了除脾细胞外，肠系膜淋巴结(MLN)细胞对刀豆蛋白A(ConA)的增殖反应。感染后第7天和第10天，与未感染的小鼠的脾细胞相比，脾细胞的增殖反应显著受到抑制(分别减少62%和91%)。相反，这些感染的小鼠的MLN细胞的增殖反应与正常的MLN细胞没有什么不同。由于干扰素-γ诱导的反应性氮中间体(RNI)的产生在抑制感染小鼠脾细胞的增殖反应中起主要作用，我们比较了感染后小鼠脾细胞和MLN细胞产生的干扰素-γ和RNI。在ConA刺激后，MLN细胞产生的干扰素-γ与脾细胞一样多，但产生的亚硝酸盐(作为衡量RNI的指标)减少了70%。当MLN细胞与感染小鼠的脾细胞共培养时，其增殖反应受到抑制，而在共培养中加入RNI抑制剂可抑制这种抑制，这表明MLN细胞减少RNI的产生有助于它们维持较高的增殖反应。这些结果表明，在感染的急性期，MLN和脾中的T细胞活性有明显的差异。
The suppression of T cell responsiveness which occurs after infection withToxoplasma gondiiin mice has been widely studied using spleen cells. Because the natural route of infection withT. gondiiis the peroral route, we examined the proliferative responses of mesenteric lymph node (MLN) cells, in addition to spleen cells, to Concanavalin‐A (Con‐A) in mice perorally infected withT. gondii.Proliferative responses of spleen cells were significantly suppressed seven and ten days after infection when compared with spleen cells from uninfected mice (62% and 91% reduction, respectively). In contrast, proliferative responses of MLN cells from these infected mice did not differ from those of normal MLN cells. Since IFN‐γ‐induced reactive nitrogen intermediate (RNI) production has been reported to play a major role in suppression of proliferative responses in spleen cells of infected mice, we compared production of IFN‐γ and RNI by spleen and MLN cells following infection. MLN cells produced as much IFN‐γ as did spleen cells, but produced 70% less nitrite (as a measure of RNI) after Con‐A stimulation. Proliferative responses of MLN cells were suppressed when co‐cultured with spleen cells from infected mice, and addition of an inhibitor of RNI to these co‐culture inhibited this suppression, suggesting that reduced RNI production by MLN cells contributes to their maintenance of higher proliferative responses. These results demonstrated a clear difference in activity of T cells in the MLN and spleen during the acute stage of the infection.