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STAT3 locus in inflammatory bowel disease and multiple sclerosis susceptibility
Genes and Immunity
|March 5, 2010
Summary
Signal transducer and activator of transcription 3 (STAT3) gene polymorphisms are linked to inflammatory bowel disease (IBD) risk, including Crohn's disease and ulcerative colitis. However, STAT3 plays a minor role in multiple sclerosis (MS) susceptibility.
Area of Science:
- Genetics
- Immunology
- Molecular Biology
Background:
- Signal transducer and activator of transcription 3 (STAT3) signaling is crucial in Th17-dependent autoimmune diseases.
- Genome-wide association studies suggest STAT3 gene involvement in inflammatory bowel disease (IBD) susceptibility.
- STAT3 activation is observed in T cells of multiple sclerosis (MS) patients.
Purpose of the Study:
- To investigate the role of STAT3 gene polymorphisms in the risk of Crohn's disease (CD), ulcerative colitis (UC), and MS.
- To validate the association of STAT3 with IBD phenotypes in an independent Spanish cohort.
Main Methods:
- Genotyping of STAT3 polymorphisms (rs3809758/rs744166/rs1026916/rs12948909) and haplotype analysis.
- Study included 860 IBD patients, 1540 MS patients, and 1720 controls from Spain.
Main Results:
- A specific STAT3 haplotype was significantly associated with increased risk for both CD (P=0.005) and UC (P=0.002).
- No significant association was found between the studied STAT3 polymorphisms and MS risk.
- The findings confirm the association of STAT3 with IBD in an independent population.
Conclusions:
- STAT3 gene polymorphisms contribute to the susceptibility of both Crohn's disease and ulcerative colitis.
- The role of STAT3 in multiple sclerosis appears to be minimal.
- This study reinforces the importance of STAT3 in IBD pathogenesis.
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