Hesse M, Bayrak S, Mitchison A
Deutsches Rheuma-Forschungs-Zentrum, Berlin, Germany.
Eur J Immunol. 1996 Dec;26(12):3234-7. doi: 10.1002/eji.1830261259.
To investigate the role of interleukin (IL)-4 during the triggering of collagen-induced arthritis, we examined the effects of the I-A(b) and I-E protective/suppressive genes and passively administered anti-IL-4 monoclonal antibody. In contrast to the action of I-E expression on its own, which has mainly a suppressive effect post-triggering, the combination of I-A(b) and I-E had a marked protective effect. Assuming, on the basis of previous experience with the I-A(b) allele, that it might act through suppressing early IL-4 production, we treated mice with the 11B11 IL-4-neutralizing antibody around the time of initial immunization with collagen. Treatment over a period extending to 6 days post-immunization exacerbated the arthritis, but when curtailed to 2 days post-immunization (and tested in pristane-primed animals), the disease was reduced. We conclude that IL-4 plays an essential role in triggering the disease.
为了研究白细胞介素（IL）-4在胶原诱导性关节炎触发过程中的作用，我们检测了I-A(b)和I-E保护性/抑制性基因的作用，并被动给予抗IL-4单克隆抗体。与I-E单独表达的作用相反，I-E单独表达主要在触发后起抑制作用，而I-A(b)和I-E的组合具有显著的保护作用。基于先前对I-A(b)等位基因的经验，假设它可能通过抑制早期IL-4的产生发挥作用，我们在初次用胶原免疫前后用11B11 IL-4中和抗体处理小鼠。免疫后持续6天的治疗加剧了关节炎，但当缩短至免疫后2天（并在 pristane 预处理的动物中进行测试）时，疾病减轻。我们得出结论，IL-4在触发该疾病中起重要作用。
