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Please use this identifier to cite or link to this item: http://hdl.handle.net/1942/9838

Title: A Single Nucleotide Polymorphism within the Interleukin-7 Receptor Alpha Promoter Influences Recent Thymic Emigrants in Multiple Sclerosis
Authors: BROUX, Bieke
Issue Date: 2009
Citation: CLINICAL IMMUNOLOGY, 131. p. S99-S100
Abstract: Recently, several new multiple sclerosis (MS) risk genes, including the interleukin-7 receptor α chain (IL-7Rα, CD127), have been identified by genome wide association studies. Since IL-7R triggering plays an important role in T cell development and survival, we postulate that polymorphisms within the IL-7Rα gene could affect T cell function in patients with MS. Therefore, we correlated the genotypes of MS patients (n=65) and healthy controls(HC, n=33) with frequencies of regulatory T cells (Treg) and expression of CD31 and CD127 in both Treg and Conventional T cells (Tconv). CD31 is a marker for recent thymic emigrants (RTE), which are characterized by high T cell receptor excision circles (TREC) and a low number of cell divisions. We found that the MS associated SNP rs6897932 does not influence the frequency of CD4+ CD25hi CD127low Tregs, nor the frequency of CD31+ T cells or expression levels of CD127 for both Tconv and Tregs. Another SNP (rs11567685; C/T) within the IL-7Rα promoter region was reported to influence the expression of CD127 on T cells of primary progressive MS patients. We found that there was a trend towards higher expression of CD127 on Tconv (p = 0.14), but not on Tregs of MS patients carrying the C allele. Strikingly, the frequency of CD31+ naïve (CD45RA+) Tconv and Tregs was significantly reduced in MS patients that are homozygous for the T allele (Tconv, p = 0.001; Tregs, p = 0.005). These results point towards a contribution of this promoter SNP to alterations in T cell development reported in MS patients.
Notes: Hasselt Univ, Diepenbeek, Belgium. Transnatl Univ Limburg, Diepenbeek, Belgium.
URI: http://hdl.handle.net/1942/9838
DOI: 10.1016/j.clim.2009.03.289
ISI #: 000266342300281
ISSN: 1521-6616
Category: M
Type: Journal Contribution
Appears in Collections: Research publications

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