T-Cell and macrophage activation in experimental autoimmune neuritis and Guillain-Barr� syndrome

Abstract

Evidence implicating cellular immune responses in the pathogenesis of experimental autoimmune neuritis (EAN) and Guillain-Barré syndrome (GBS) is reviewed. In EAN the decisive role of T-lymphocytes in the initiation of immune-mediated nerve damage has been firmly established by adoptive transfer experiments. Macrophages but not Schwann cells express major histocompatibility complex class II gene products in situ and hence may function as antigen presenters. Macrophages are crucial in the amplification and effector phase and damage the myelin sheath by phagocytic attack and release of inflammatory mediators such as toxic oxygen radicals, arachidonic acid metabolites, complement, or hydrolases. Macrophage activation in EAN is achieved by interferon-gamma. Attempts to detect specific sensitization of T-lymphocytes to nerve antigens in patients with GBS have so far been unsuccessful. However, circulating activated T cells can be found in patients with GBS, as evidenced by augmented expression of HLA-DR antigen, the transferrin receptor, and the interleukin-2 receptor on the surface of peripheral blood T cells, and by increased serum concentrations of interleukin-2 and the soluble interleukin-2 receptor. In addition, we present data indicating macrophage activation in GBS.