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

Chemokines are low molecular weight chemotactic peptides that bind seven tr ansmembrane-spanning, G protein-coupled receptors and deliver signals leadi ng to T cell costimulation, hematopoeisis, cytokine expression, T cell diff erentiation, and integrin activation. Experimental autoimmune encephalomyel itis (EAE) is a CD4(+) Th1-mediated demyelinating disease of the central ne rvous system (CNS) that serves as a model for multiple sclerosis (MS). A ha llmark in the pathogenesis of this CNS demyelinating disease is the emigrat ion of T cells and monocytes from the blood to the CNS. There are several c onsiderations that suggest a role for chemokines in the influx of inflammat ory cells and the resulting disease process including a tight temporal expr ession pattern with relationship to disease activity and prevention of dise ase development by in. vivo neutralization. We review the evidence that tem poral and spatial expressions of chemokines are crucial factors, complement ing adhesion molecule upregulation, that regulate EAE and potentially MS di sease activity as well as the functions of chemokines in Th1 and Th2 biolog y.