Host protective antibodies and serum immunoglobulin isotypes in mice chronically infected or repeatedly immunized with the nematode parasite Nematospiroides dubius.
Host protective antibodies and serum immunoglobulin isotypes in mice chronically infected or repeatedly immunized with the nematode parasite Nematospiroides dubius.
复制标题
慢性感染或反复免疫线虫寄生虫疑似线虫的小鼠体内的宿主保护性抗体和血清免疫球蛋白同种型。
作者：
D. Williams;J. Behnke
线虫寄生虫Nematospiroides pneumonus存活，在小鼠中引起慢性原发感染。然而，每周感染125只幼虫的小鼠，通过驱虫剂治疗以防止肠道内累积致死数量蠕虫，在其血清中产生宿主保护性抗体。这些抗体的保护作用通过被动转移到幼稚受体或已经用免疫肠系膜淋巴结细胞（IMLNC）过继免疫的小鼠来证明。血清首次显示在多重免疫感染的第三和第四周期间表现出保护活性，在第六周达到峰值水平，超过该峰值，保护活性没有进一步增加。这种增加与血清IgG 1水平同时升高10倍相关。其他免疫球蛋白同种型均未发生类似的浓度变化，也不能与供体小鼠血清中宿主保护性抗体的出现模式相关。这表明宿主保护性抗体为IgG 1类。CFLP和C57 BL 10小鼠（后者是弱应答品系）的血清中都有高水平的宿主保护性抗体。然而，当比较来自NIH小鼠（强应答品系）的血清时，它们在被动转移至受体小鼠时表现出少得多的保护活性，尽管当与IMLNC一起给予时，来自多重免疫NIH小鼠的血清协同地增强了IMLNC的保护作用。当在该被动/过继转移模型中测定原发感染血清时，即使在感染后10周和17周采集原发感染血清池，也不能证明宿主保护性抗体。这些结果进行了讨论的可能机制，N。Escherichia coli逃避宿主免疫系统，在小鼠中引起持久的原发性感染。
The nematode parasite Nematospiroides dubius survives to give a chronic primary infection in mice. However, mice subjected to weekly infections of 125 larvae, interspersed by treatment with an anthelmintic to prevent the accumulation of lethal numbers of adult worms in the intestine, develop host-protective antibodies in their serum. The protective effect of these antibodies was demonstrated by passive transfer to naive recipients or to mice already adoptively immunized with immune mesenteric lymph node cells (IMLNC). Sera were first shown to exhibit protective activity during the third and fourth weeks of the multiple immunizing infection, reaching a peak level by week six beyond which there was no further increase in protective activity. This increase was correlated with a ten-fold, concurrent rise in serum IgG1 levels. None of the other immunoglobulin isotypes underwent comparable changes in concentration nor could they be correlated with the pattern of appearance of host-protective antibodies in the sera of donor mice. This suggested that host protective antibodies were of the IgG1 class. CFLP and C57BL10 mice (the latter is a weak responder strain) both had high levels of host-protective antibodies in their serum. However when the sera from NIH mice (a strong responder strain) were compared, they exhibited far less protective activity on passive transfer to recipient mice, although when given together with IMLNC, serum from multiply-immunized NIH mice enhanced the protective effect of IMLNC synergistically. When primary infection serum was assayed in this passive/adoptive transfer model, no host-protective antibodies could be demonstrated, even with pools of primary infection serum taken 10 and 17 weeks after infection. These results are discussed with respect to the possible mechanisms by which N. dubius evades the host immune system to give rise to long-lasting primary infections in mice.