Koyama K, Tamauchi H, Tomita M, Kitajima T, Ito Y
Department of Parasitology, Kitasato University School of Medicine, Kanagawa, Japan.
Parasitol Res. 1999 Mar;85(3):194-9. doi: 10.1007/s004360050534.
Immune responses in resistant BALB/c mice infected with the murine nematode parasite Trichuris muris were examined. Following the establishment of infection, worm burdens of T. muris were expelled by BALB/c mice by day 21 postinfection (p.i.). Specific immunoglobulin G1 (IgG1) antibodies to T. muris excretory/secretory (E/S) antigens were detected in sera from infected mice, though specific IgG2a antibodies were not observed during infection. Ig-producing cells increased in the mesenteric lymph nodes (MLN) of infected mice on days 7, 14, and 21 p.i., with the greatest increase in numbers of IgG- and IgA-producing cells occurring on day 14. Marked increases in the relative percentages of B220+ and surface Ig+ (sIg+) cells were observed in the MLN of infected mice on days 14 and 21 p.i. Furthermore, cellular expansion of the MLN in infected mice resulted in an increase in the absolute numbers of B220+ and sIg+ cells. The levels of interleukin 2 (IL-2), IL-4, and interferon-gamma (IFN-gamma) detected in the supernatants from concanavalin A-stimulated MLN cells of infected mice were higher than those found in normal mice. Consequently, the expulsion of T. muris in resistant BALB/c mice was concomitant with cytokine production and B-cell activation in the MLN of infected mice. These results suggest the involvement of B-cell responses in protective immunity to T. muris infection.
对感染鼠类线虫寄生虫毛首鞭形线虫的抗性BALB/c小鼠的免疫反应进行了研究。感染确立后,毛首鞭形线虫的虫负荷在感染后第21天被BALB/c小鼠排出。在感染小鼠的血清中检测到针对毛首鞭形线虫排泄/分泌(E/S)抗原的特异性免疫球蛋白G1(IgG1)抗体,不过在感染期间未观察到特异性IgG2a抗体。在感染后第7天、14天和21天,感染小鼠肠系膜淋巴结(MLN)中产生Ig的细胞增加,其中产生IgG和IgA的细胞数量在第14天增加最多。在感染后第14天和21天,感染小鼠的MLN中观察到B220+和表面Ig+(sIg+)细胞的相对百分比显著增加。此外,感染小鼠MLN的细胞扩增导致B220+和sIg+细胞的绝对数量增加。在感染小鼠的伴刀豆球蛋白A刺激的MLN细胞上清液中检测到的白细胞介素2(IL-2)、IL-4和干扰素-γ(IFN-γ)水平高于正常小鼠。因此,抗性BALB/c小鼠中毛首鞭形线虫的排出与感染小鼠MLN中的细胞因子产生和B细胞活化同时发生。这些结果表明B细胞反应参与了对毛首鞭形线虫感染的保护性免疫。