Affordable Access

Role of chemokines in the regulation of Th1/Th2 and autoimmune encephalomyelitis.

Authors
  • Kennedy, K J
  • Karpus, W J
Type
Published Article
Journal
Journal of Clinical Immunology
Publisher
Springer Nature
Publication Date
Sep 01, 1999
Volume
19
Issue
5
Pages
273–279
Identifiers
PMID: 10535603
Source
Medline
License
Unknown

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.

Report this publication

Statistics

Seen <100 times