Authors: Yousefipour, G.¹; Erfani, N.²; Momtahan, M.¹; Moghaddasi, H.¹; Ghaderi, A.²

Source: Acta Neurologica Scandinavica, Volume 120, Number 6, December 2009 , pp. 424-429(6)

Publisher: Wiley-Blackwell

Abstract:

Yousefipour G, Erfani N, Momtahan M, Moghaddasi H, Ghaderi A. CTLA4 exon 1 and promoter polymorphisms in patients with multiple sclerosis.

Acta Neurol Scand 2009: 120: 424-429.

© 2009 The Authors Journal compilation © 2009 Blackwell Munksgaard. Objective - 

The polymorphisms of exon 1 (+49 A/G) and promoter regions (−1722 T/C, −1661 A/G and −318 C/T)of cytotoxic T lymphocyte antigen 4 (CTLA4) and also haplotypes constructed from mentioned loci were investigated amongst 153 Iranian patients with definite multiple sclerosis (MS) and 190 healthy controls. Methods - 

The polymorphisms were genotyped by PCR-restriction fragment length polymorphisms and PCR-amplification refractory mutation system. The 4-locus haplotypes were estimated by Arlequin software (University of Berne, Berne, Switzerland). Results - 

Preliminary results showed significant increase of +49 G allele and −1661 AG genotype, as well as TGCA haplotype among patients than controls (P < 0.036, P = 0.009 and P < 0.010, respectively). The distribution of −1722 T/C, −1661 A/G, −318 C/T and +49 A/G (TACA) haplotype, from the contrary, was observed to be significantly increased among controls (P < 0.001). Conclusions - 

After Bonferroni correction, the results provide preliminary evidence that CTLA4 genetic variation at −1661 locus may render Iranian individuals to be more susceptible to MS, whereas harboring TACA haplotype might be protective.

Keywords: −1661 A/G; cytotoxic T lymphocyte antigen 4; exon 1; haplotype; multiple sclerosis; polymorphism

Document Type: Research article

DOI: http://dx.doi.org/10.1111/j.1600-0404.2009.01177.x

Affiliations: 1: Department of Neurology, Shiraz University of Medical Sciences, Shiraz, Iran 2: Shiraz Institute for Cancer Research, Shiraz University of Medical Sciences, Shiraz, Iran

Publication date: 2009-12-01

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