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Related Experiment Video

Updated: May 8, 2026

Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes

Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes

Published on: September 26, 2013

IL7RA haplotype-associated alterations in cellular immune function and gene expression patterns in multiple

J Jäger¹, C Schulze, S Rösner

¹Institute for Neuroimmunology and Clinical Multiple Sclerosis Research (inims), Centre for Molecular Neurobiology Hamburg (ZMNH), University Medical Centre Hamburg-Eppendorf, Hamburg, Germany.

Genes and Immunity

|August 30, 2013

Summary

Genetic variations in Interleukin-7 receptor alpha (IL7RA) influence multiple sclerosis (MS) risk. Protective IL7RA haplotypes are linked to lower soluble IL7RA (sIL-7RA) levels, affecting T cell responses.

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Microbiota Analysis Using Two-step PCR and Next-generation 16S rRNA Gene Sequencing

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Area of Science:

Immunology
Genetics
Neuroscience

Background:

Interleukin-7 receptor alpha (IL7RA) is a key gene associated with multiple sclerosis (MS) susceptibility.
Soluble IL-7RA (sIL-7RA) levels and mRNA expression differ across common IL7RA haplotypes.

Purpose of the Study:

To investigate the functional impact of IL7RA genetic variants on sIL-7RA levels and T cell responsiveness in MS.
To explore how different IL7RA haplotypes influence immune cell gene expression patterns.

Main Methods:

Serum sIL-7RA levels were measured and correlated with IL7RA haplotypes.
IL-7-mediated STAT5 phosphorylation in CD4(+) T cells was assessed.
Transcriptome analysis was performed on CD4(+) T cells from MS patients with varying IL7RA haplotypes.

Main Results:

Individuals with protective IL7RA haplotypes exhibited significantly lower serum sIL-7RA levels (threefold reduction).
Elevated sIL-7RA concentrations impaired IL-7-induced STAT5 phosphorylation in CD4(+) T cells.
Distinct gene expression profiles were observed in CD4(+) T cells based on IL7RA haplotypes, involving cytokine signaling, apoptosis, and cell cycle pathways.

Conclusions:

IL7RA genetic variants influence MS susceptibility through haplotype-associated differences in sIL-7RA levels and immune cell responses.
The impact of IL7RA on MS risk extends beyond sIL-7RA levels, involving complex alterations in immune cell function.