Clayton C E, Ogilvie B M, Askonas B A
Parasite Immunol. 1979 Spring;1(1):39-48. doi: 10.1111/j.1365-3024.1979.tb00694.x.
B lymphocyte function was assessed in outbred nude mice and nu/+controls infected with Trypanosoma brucei brucei. On day 10 of the infection in outbred nu/nu mice in which the initial wave of parasites was strongly controlled, B cell function was unaltered on enhanced compared with uninfected animals or infected nu/+. In other nu/nu mice unable to control the initial parasitaemia, thymidine incorporation and Ig secretion by spleen cells were increased on day 10 and their response to lipopolysaccharide in vitro negated. By day 15 however, even the spleen cells of infected nu/nu which controlled the initial wave of parasites were proliferating and secreting Ig on removal from the mice and they were unable to respond to LPS in vitro. These experiments confirm results of a previous study of B cell function in T cell-depleted mice (Askonas et al. 1979). T. b. brucei infection of mice causes both enhanced Ig production and suppression of the ability of B cells to respond to mitogen even in the absence of T cells, but the presence of T cells may accelerate the changes which occur in B lymphocytes following this infection.
在感染布氏布氏锥虫的远交系裸鼠和杂合子对照小鼠中评估了B淋巴细胞功能。在远交系裸鼠感染的第10天，最初一波寄生虫受到强烈控制，与未感染动物或感染的杂合子相比，B细胞功能未改变或增强。在其他无法控制初始寄生虫血症的裸鼠中，脾细胞的胸腺嘧啶核苷掺入和Ig分泌在第10天增加，并且它们在体外对脂多糖的反应被消除。然而到第15天，即使是那些控制了最初一波寄生虫的感染裸鼠的脾细胞，在从小鼠体内取出后也开始增殖并分泌Ig，并且它们在体外无法对LPS作出反应。这些实验证实了先前一项关于T细胞缺陷小鼠B细胞功能研究的结果（Askonas等人，1979年）。小鼠感染布氏布氏锥虫即使在没有T细胞的情况下也会导致Ig产生增强以及B细胞对有丝分裂原反应能力的抑制，但T细胞的存在可能会加速这种感染后B淋巴细胞中发生的变化。
