| Literature DB >> 11108946 |
Y C Zang1, J B Halder, A K Samanta, J Hong, V M Rivera, J Z Zhang.
Abstract
Trafficking of inflammatory T cells into the brain is associated with interactions of certain chemokines with their receptors, which plays an important role in the pathogenesis of multiple sclerosis (MS). We examined whether interferon-beta (IFN-beta) had the ability to regulate the production of chemokines and the expression of their receptors in T cells derived from patients with MS. It was demonstrated for the first time that in vitro exposure of T cells to IFN-beta-1a selectively inhibited mRNA expression for RANTES and MIP-1alpha and their receptor CCR5. T cell surface expression of CCR5 was significantly reduced in MS patients treated with IFN-beta, correlating with decreased T cell transmigration toward RANTES and MIP-1alpha. The study provides new evidence suggesting that IFN-beta treatment impairs chemokine-induced T cell trafficking by reducing the production of RANTES and MIP-1alpha and the expression of their receptors CCR5.Entities:
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Year: 2001 PMID： 11108946 DOI： 10.1016/s0165-5728(00)00397-0
Source DB: PubMed Journal: J Neuroimmunol ISSN： 0165-5728 Impact factor: 3.478