Kobayashi Y, Kawai K, Honda H, Tomida S, Niimi N, Tamatani T, Miyasaka M, Yoshikai Y
Department of Neurology, Nagoya University School of Medicine, Japan.
Cell Immunol. 1995 Sep;164(2):295-305. doi: 10.1006/cimm.1995.1173.
We obtained the evidence that coadministration in vivo of mAbs against leukocyte function-associated antigen-1 (LFA-1) and intercellular adhesion molecule-1 (ICAM-1) suppressed the progression of experimental allergic encephalomyelitis (EAE) in rats. The suppressive effect in vivo of coadministration of the mAbs during the induction phase was not prominent, but the administration of these mAbs during the effector phase markedly suppressed the progression of clinical illness and prevented the infiltration of encephalitogenic cells into the central nervous system. However, administration of the mAb to LFA-1 alone or ICAM-1 alone did not show such suppressive effects. These findings suggest that LFA-1 and ICAM-1 are critically involved in the development of EAE and that the administration together of mAbs against adhesion molecules including LFA-1 and ICAM-1 might provide a new immunotherapeutic approach for the treatment of multiple sclerosis.
我们获得的证据表明，在体内共同给予抗白细胞功能相关抗原-1（LFA-1）和细胞间黏附分子-1（ICAM-1）的单克隆抗体可抑制大鼠实验性自身免疫性脑脊髓炎（EAE）的进展。在诱导期共同给予单克隆抗体的体内抑制作用不显著，但在效应期给予这些单克隆抗体可显著抑制临床疾病的进展，并阻止致脑炎细胞浸润到中枢神经系统。然而，单独给予抗LFA-1或抗ICAM-1单克隆抗体并未显示出这种抑制作用。这些发现表明，LFA-1和ICAM-1在EAE的发生发展中起关键作用，并且共同给予针对包括LFA-1和ICAM-1在内的黏附分子的单克隆抗体可能为治疗多发性硬化症提供一种新的免疫治疗方法。
