Journal of Clinical Immunology

, Volume 19, Issue 5, pp 273–279

Role of Chemokines in the Regulation of Th1/Th2 and Autoimmune Encephalomyelitis

  • Kevin J. Kennedy
  • William J. Karpus
Article

DOI: 10.1023/A:1020535423465

Cite this article as:
Kennedy, K.J. & Karpus, W.J. J Clin Immunol (1999) 19: 273. doi:10.1023/A:1020535423465

Abstract

Chemokines are low molecular weight chemotactic peptides that bind seven transmembrane-spanning, G protein-coupled receptors and deliver signals leading to T cell costimulation, hematopoeisis, cytokine expression, T cell differentiation, and integrin activation. Experimental autoimmune encephalomyelitis (EAE) is a CD4+ Th1-mediated demyelinating disease of the central nervous system (CNS) that serves as a model for multiple sclerosis (MS). A hallmark in the pathogenesis of this CNS demyelinating disease is the emigration of T cells and monocytes from the blood to the CNS. There are several considerations that suggest a role for chemokines in the influx of inflammatory cells and the resulting disease process including a tight temporal expression pattern with relationship to disease activity and prevention of disease development by in vivo neutralization. We review the evidence that temporal and spatial expressions of chemokines are crucial factors, complementing adhesion molecule upregulation, that regulate EAE and potentially MS disease activity as well as the functions of chemokines in Th1 and Th2 biology.

Experimental autoimmune encephalomyelitismultiple sclerosischemokinereviewautoimmunityT helper cells

Copyright information

© Plenum Publishing Corporation 1999

Authors and Affiliations

  • Kevin J. Kennedy
    • 1
  • William J. Karpus
    • 1
  1. 1.Department of Pathology, Immunobiology Center, Robert H. Lurie Cancer Center, and Institute for NeuroscienceNorthwestern University Medical SchoolChicago
  2. 2.Department of PathologyNorthwestern University Medical SchoolChicago