Scand J Immunol. 2003 Jul;58(1):81-8
Glabinski AR, Bielecki B, Ransohoff RM.
Department of Neurology, Medical University of Lodz, ul. Kopcinskiego, Lodz, Poland; and Department of Neurosciences, Cleveland Clinic Foundation, Euclid Avenue, Cleveland, OH, USA.
Chronic relapsing experimental autoimmune encephalomyelitis (ChREAE) is an autoimmune disease of the central nervous system (CNS) induced by CNS myelin components.
In the early active stage, both ChREAE and multiple sclerosis (MS) are characterized by the presence of perivascular inflammatory cuffs disseminated in the CNS.
There is growing evidence that chemoattractant cytokines (chemokines) play an important role in this process.
The main goal of the present study was to analyse the hypothesis that chemokine expression in the CNS during autoimmune inflammation is regulated by proinflammatory cytokines.
To address this concept, we analysed temporal relations between chemokine and cytokine expression during ChREAE.
Phasic upregulation of gene expression for chemokines T-cell activation gene 3 (TCA-3)/CCL1, monocyte chemoattractant protein-1 (MCP-1)/CCL2, macrophage inflammatory protein-1 alpha (MIP-1alpha)/CCL3, MIP-1beta/CCL4, regulated on activation normal T cell expressed and secreted (RANTES)/CCL5 and MIP-2/CXCL2-3 as well as cytokines tumour necrosis factor-alpha (TNF-alpha), -beta, LT-beta, interferon-gamma (IFN-gamma) and transforming growth factor-beta1 (TGF-beta1) in the CNS was observed during attacks of ChREAE.
Expression of cytokines TNF-beta and LT-beta preceded, and the expression of TGF-beta1 followed chemokine upregulation.
Our results suggest that chemokine expression during CNS autoimmune inflammation may be regulated by some proinflammatory cytokines.