Yoshino S
Department of Microbiology, Saga Medical School, Nabeshima, Japan.
Br J Pharmacol. 1998 Jan;123(2):237-42. doi: 10.1038/sj.bjp.0701607.
1 The present study was undertaken to investigate the effect of a monoclonal antibody (11B11 mAb) against interleukin-4 (IL-4) on collagen-induced arthritis (CIA) in mice. 2 11B11 mAb was daily injected intraperitoneally over a period of 10 days, commencing on the day of immunization with type II collagen (CII). 3 The results showed that the anti-IL-4 mAb markedly augmented both the incidence and the severity of CIA. The augmentation of the disease was associated with a significant increase in anti-CII IgG2a antibody production, proliferative responses of lymph node cells to CII and interferon-gamma (IFN-gamma) secretion from the lymphoid cells. The production of anti-CII IgG1 antibodies the secretion of IL-4 was markedly reduced in the mAb-treated mice. 4 Thus, the neutralization of IL-4 by 11B11 mAb appears to be effective in augmenting CIA.
1 本研究旨在探讨抗白细胞介素-4(IL-4)单克隆抗体(11B11 mAb)对小鼠胶原诱导性关节炎(CIA)的影响。2 从用II型胶原(CII)免疫当天开始,连续10天每天腹腔注射11B11 mAb。3 结果显示,抗IL-4 mAb显著增加了CIA的发病率和严重程度。疾病的加重与抗CII IgG2a抗体产生的显著增加、淋巴结细胞对CII的增殖反应以及淋巴细胞分泌干扰素-γ(IFN-γ)有关。在mAb处理的小鼠中,抗CII IgG1抗体的产生和IL-4的分泌明显减少。4 因此,11B11 mAb对IL-4的中和作用似乎在增强CIA方面有效。