It has been speculated that b-chemokines play a pivotal role in the development of peripheral nervous system (PNS) disorders characterized by mononuclear cell in®ltration. In experimental allergic neuritis (EAN), an animal model for human Guillain-Barre  syndrome (GBS) with mononuclear cell in®ltration, we found by quantitative PCR that b-chemokine messages were upregulated during the active stage. Moreover, an increase in the monocyte chemoattractant protein-1 (MCP-1) message was found in the preclinical stage of EAN, suggesting the critical role of MCP-1 for inducing mononuclear cell in®ltrations in this model. Since many cell lineages other than immune cells can produce chemokines, this early upregulation of MCP-1 may be mediated by non-immune cells, probably endothelia or Schwann cells. To date, apart from MCP-1, only RANTES (Regulated on activation, normal T cell expressed and secreted) and macrophage in¯ammatory protein (MIP)-1a have been examined in EAN and found to have similar kinetics of induction. Therefore, understanding the regulation of production of these chemokines as well as mechanisms of inhibiting chemokine/receptor interactions in the PNS may ultimately lead to disease-speci®c therapy for GBS and related demyelinating disorders.