Chemokine actions in the CNS: Insights from transgenic mice

Abstract

Historically the central nervous system (CNS) has been viewed as a relatively immune sheltered tissue. Under physiological conditions the CNS is devoid of leukocytes, including professional antigen presenting cells (APC), is deficient in key immune accessory molecules such as major histocompatibility molecules (MHC) and is protected by an effective blood brain barrier. Significantly, however, in numerous pathological states including infectious diseases and autoimmune disorders (e.g. multiple sclerosis) immune cells are effectively recruited to and infiltrate in the CNS. This immune response can be a two-edged sword required on the one hand to control infection and facilitate tissue repair and regeneration but on the other causing tissue injury that can result in life threatening complications. Therefore, understanding the mechanisms that control the trafficking of leukocytes to the CNS and the subsequent interactions between these cells that contribute to tissue injury has significant implications. © 2008 Springer.