
Vol. 52, No. 3, 2004
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Original Paper
Expression of Th1/Th2-Related Chemokine Receptors on Peripheral T Cells and Correlation with Clinical Disease Activity in Patients with Multiple Sclerosis
Hideto Nakajimaa, Kazuhiro Fukudaa, Yoshimitsu Doia, Masakazu Suginoa, Fumiharu Kimuraa, Toshiaki Hanafusaa, Toshiyuki Ikemotob, Akira Shimizub
aDivision of Neurology, First Department of Internal Medicine, and bDepartment of Central Laboratory, Osaka Medical College, Takatsuki City, Japan
Address of Corresponding Author
Eur Neurol 2004;52:162-168 (DOI: 10.1159/000081856)
Key Words
- Multiple sclerosis
- Chemokine
- Chemokine receptor
- Th1
- Th2
Abstract
Th1 cells play an important role in the pathogenesis of multiple sclerosis (MS), a disease likely linked to an autoimmune process. We measured the levels of chemokines in serum or cerebrospinal fluid (CSF) samples by ELISA, and also studied the expression of Th1-related CXCR3/CCR5 chemokine receptors and Th2-related CCR4/CCR3 chemokine receptors on blood cells from MS patients using three-color flow cytometry. The Bonferroni correction was used for the statistical analysis. The levels of CXCL10, CCL3, and CCL5 in the CSF samples for the MS groups were significantly higher than those for the control group. However, the levels of CCL2 in both the CSF and serum samples for the remission group were significantly higher than those for the active group. The percentage of CXCR3-expressing CD4+ T cells in patients with MS was significantly elevated compared with the healthy controls. Moreover, MS patients in an active phase showed a more increased CD4+CXCR3+/CD4+CCR4+ ratio than patients in a remission phase. The increased percentage of CD4+CXCR3+ cells in the blood was associated with relapses in MS. This study suggested that the CD4+CXCR3+/CD4+CCR4+ ratio could be a sensitive maker of immune dysfunction in MS. Copyright © 2004 S. Karger AG, Basel
Author Contacts
Hideto Nakajima, MD Division of Neurology, First Department of Internal Medicine, Osaka Medical College 2-7 Daigakumachi Takatsuki City, Osaka 569-8686 (Japan) Tel. +81 72 683 1221, Fax +81 72 683 1801, E-Mail in1045@poh.osaka-med.ac.jp
Article Information
Received: January 13, 2004
Accepted: August 31, 2004
Published online: November 2, 2004
Number of Print Pages : 7
Number of Figures : 4, Number of Tables : 0, Number of References : 19 |
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