Abstract
Apolipoprotein E (apoE) has immunomodulatory properties and has been implicated in the pathogenic mechanism of autoimmune diseases. Previously, the authors found that apoE deficiency increased the susceptibility to experimental autoimmune neuritis (EAN), an animal model for human Guillain‐Barré syndrome. To further elucidate the mechanism behind apoE deficiency exacerbating EAN, the authors investigated the role of major target and important antigen‐presenting cells of the peripheral nerve system, Schwann cells (SCs), in apoE knockout mice. Treatment of apoE deficient SCs with recombinant mouse interferon‐γ and lipopolysaccharide resulted in higher MHC‐II and CD40 expression as compared with normal SCs derived from wild‐type mice. The increased MHC‐II and CD40 expression on SCs was accompanied by lower levels of intracellular IL‐6 production within SCs of apoE deficiency, which is confirmed by the neutralization with anti IL‐6 antibody. The increased antigen‐presenting capacity of apoE deficient SCs was further explored by enhancement of T cell proliferation co‐cultured with P0 peptide 180–199 specific T cells derived from EAN mice immunized with the P0 peptide. In conclusion, apoE may protect mice from EAN and probably also from chronic inflammatory demyelinating polyneuropathy by affecting the antigen‐presenting function of SCs via influence of IL‐6 production. © 2007 Wiley‐Liss, Inc.