ANTIBODIES AGAINST LEUKOCYTE FUNCTION-ASSOCIATED ANTIGEN-1 AND AGAINST INTERCELLULAR-ADHESION MOLECULE-1 TOGETHER SUPPRESS THE PROGRESSION OF EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS

被引:51
|
作者
KOBAYASHI, Y
KAWAI, K
HONDA, H
TOMIDA, S
NIIMI, N
TAMATANI, T
MIYASAKA, M
YOSHIKAI, Y
机构
[1] NAGOYA UNIV,SCH MED,DEPT ORAL SURG,NAGOYA,AICHI 466,JAPAN
[2] NAGOYA UNIV,SCH MED,DIS MECHANISM & CONTROL RES INST,GERMFREE LIFE LAB,NAGOYA,AICHI 466,JAPAN
[3] JT INC,PHARMACEUT BASIC RES LAB,TOKYO 113,JAPAN
[4] OSAKA UNIV,SCH MED,BIOMED RES CTR,DEPT BIOREGULAT,OSAKA 565,JAPAN
关键词
D O I
10.1006/cimm.1995.1173
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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. (C) 1995 Academic Press, Inc.
引用
收藏
页码:295 / 305
页数:11
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