alexa Lack of Correlation between CCL5 -28C/G Functional Poly
ISSN: 2155-9899

Journal of Clinical & Cellular Immunology
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Research Article

Lack of Correlation between CCL5 -28C/G Functional Polymorphism and Multiple Sclerosis in Tunisian Patients

Nadia Ben-Fredj1, Walid Ben-Selma2*, Saber Chebel3, Mahbouba Frih-Ayed3, Mahmoud Letaief1, Aouni Mahjoub1 and Jalel Boukadida2
1Laboratory of Transmissible Diseases and Biological Active substances, LR99-ES27, Faculty of Pharmacy, University of Monastir, Avicenne street 5000, Monastir, Tunisia
2Laboratory of Microbiology and Immunology, UR02SP13, Farhat Hached University Hospital, Sousse, Tunisia
3Department of Neurology, Fattouma Bourguiba University Hospital, Monastir, Tunisia
Corresponding Author : Dr. Walid Ben-Selma
Microbiology and Immunology Laboratory, UR02SP13
CHU Farhat Hached - Av. Ibn el Jazzar- 4000, Sousse, Tunisia
Tel: +216 73219504
Fax: +216 73219504
E-mail: [email protected]
Received: April 16, 2012; Accepted: June 19, 2012; Published: June 29, 2012
Citation: Ben-Fredj N, Ben-Selma W, Chebel S, Frih-Ayed M, Letaief M, et al. (2012) Lack of Correlation between CCL5 -28C/G Functional Polymorphism and Multiple Sclerosis in Tunisian Patients. J Clin Cell Immunol 3:122. doi:10.4172/2155-9899.1000122
Copyright: © 2012 Ben-Fredj N, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Multiple sclerosis is a chronic demyelinating disease of the human central nervous system (CNS) of a still
unknown etiology. CCL5 is localized in white matter tracts undergoing demyelination, suggesting that this chemokine participates in the pathogenesis of disease by attracting inflammatory cells into the CNS. The CCL5 -28C/G functional polymorphism have been reported to be associated with multiple sclerosis, however, evidence remains conflicting. In the current study, we investigated distibution of the CCL5 -28C/G in 51 patients with multiple sclerosis in comparison to 162 healthy blood donors. The data revealed no significant differences in the distribution of the CCL5-28C/G polymorphism in multiple sclerosis patients compared with the control group. To conclude, our study showed no association between CCL5 -28C/G polymorphism and risk development of multiple sclerosis in Tunisian patients.


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