Log on / register
Feedback | Support | My details
Open AccessResearch article

An examination of the Apo-1/Fas promoter Mva I polymorphism in Japanese patients with multiple sclerosis

Masaaki Niino1 email, Seiji Kikuchi1 email, Toshiyuki Fukazawa2 email, Ryuji Miyagishi1 email, Ichiro Yabe1 email and Kunio Tashiro1 email

1Department of Neurology, Hokkaido University Graduate School of Medicine, Kita-15 Nishi-7, Kita-ku, Sapporo, 060-8638, Japan

2Hokuyukai Neurology Hospital, Niju-Yon-Ken 2-2-4-30, Nishi-ku, Sapporo, 063-0802, Japan

author email corresponding author email

BMC Neurology 2002, 2:8doi:10.1186/1471-2377-2-8

Published: 21 August 2002

Abstract

Background

The Apo-1/Fas (CD95) molecule is an apoptosis-signaling cell surface receptor belonging to the tumor necrosis factor (TNF) receptor family. Both Fas and Fas ligand (FasL) are expressed in activated mature T cells, and prolonged cell activation induces susceptibility to Fas-mediated apoptosis. The Apo-1/Fas gene is located in a chromosomal region that shows linkage in multiple sclerosis (MS) genome screens, and studies indicate that there is aberrant expression of the Apo-1/Fas molecule in MS.

Methods

Mva I polymorphism on the Apo-1/Fas promoter gene was detected by PCR-RFLP from the DNA of 114 Japanese patients with conventional MS and 121 healthy controls. We investigated the association of the Mva I polymorphism in Japanese MS patients using a case-control association study design.

Results

We found no evidence that the polymorphism contributes to susceptibility to MS. Furthermore, there was no association between Apo-1/Fas gene polymorphisms and clinical course (relapsing-remitting course or secondary-progressive course). No significant association was observed between Apo-1/Fas gene polymorphisms and the age at disease onset.

Conclusions

Overall, our findings suggest that Apo-1/Fas promoter gene polymorphisms are not conclusively related to susceptibility to MS or the clinical characteristics of Japanese patients with MS.


© 1999-2008 BioMed Central Ltd unless otherwise stated