Stoll G, Jander S, Jung S, Archelos J, Tamatani T, Miyasaka M, Toyka K V, Hartung H P
Department of Neurology, Heinrich-Heine-Universität, Düsseldorf, Germany.
Lab Invest. 1993 Jun;68(6):637-44.
Intercellular adhesion molecule-1 (ICAM-1) plays an important role in immune responses, especially in T cell/endothelial cell and T cell/macrophage interactions. This study reports the cellular localization of ICAM-1 during immune-mediated demyelination of the peripheral nervous system induced by adoptive transfer of P2 specific T cells.
Cryosections 1 micron thick of ventral roots of rats with experimental autoimmune neuritis were labeled with a monoclonal antibody against rat ICAM-1.
Numerous ICAM-1 positive cells were present before and shortly after the onset of clinical disease from days 4 to 6 after cell transfer. By day 8, their number had greatly decreased. ICAM-1 positive infiltrating cells could be identified as ED1 positive macrophages. Moreover, endothelial cells expressed ICAM-1. Schwann cells and T cells were ICAM-1 negative. While at early stages of experimental autoimmune neuritis, ICAM-1 and Ia colocalized on macrophages but not endothelial cells, Ia persisted for a longer period in nerve roots than ICAM-1. After nerve transection, macrophages entering the distal stump and endothelial cells did not express ICAM-1.
The presence of ICAM-1 immunoreactivity in peripheral nerve indicates an underlying immune-mediated process. Among other cytokines interferon-gamma, which is transiently expressed in nerves during immune-mediated demyelination but not after nerve transection, could be one mediator that induces ICAM-1 in immune-mediated demyelination of the peripheral nervous system.
细胞间黏附分子-1(ICAM-1)在免疫反应中起重要作用,尤其在T细胞/内皮细胞和T细胞/巨噬细胞相互作用中。本研究报道了在通过P2特异性T细胞的过继转移诱导的外周神经系统免疫介导的脱髓鞘过程中ICAM-1的细胞定位。
用抗大鼠ICAM-1的单克隆抗体标记患有实验性自身免疫性神经炎大鼠腹根的1微米厚冰冻切片。
在细胞转移后第4至6天临床疾病发作之前和之后不久,存在大量ICAM-1阳性细胞。到第8天,其数量已大大减少。ICAM-1阳性浸润细胞可鉴定为ED1阳性巨噬细胞。此外,内皮细胞表达ICAM-1。雪旺细胞和T细胞为ICAM-1阴性。在实验性自身免疫性神经炎的早期阶段,ICAM-1和Ia在巨噬细胞上共定位,但在内皮细胞上不共定位,Ia在神经根中的持续时间比ICAM-1长。神经横断后,进入远端残端的巨噬细胞和内皮细胞不表达ICAM-1。
外周神经中ICAM-1免疫反应性的存在表明存在潜在的免疫介导过程。在其他细胞因子中,γ干扰素在免疫介导的脱髓鞘过程中在神经中短暂表达,但在神经横断后不表达,它可能是在周围神经系统免疫介导的脱髓鞘过程中诱导ICAM-1的一种介质。