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Comprehensive Autopsy Program for Individuals with Multiple Sclerosis
Published on: July 19, 2019
The Putative Association of TOB1-AS1 Long Non-coding RNA with Immune Tolerance: A Study on Multiple Sclerosis
Reyhaneh Dehghanzad1, Majid Pahlevan Kakhki1, Asieh Alikhah1
1Department of Genetics, Faculty of Biological Sciences, Tarbiat Modares University, P.O. Box: 14115-154, Tehran, Iran.
This study reveals altered expression of the TOB1-AS1 long non-coding RNA (lncRNA) and associated genes in multiple sclerosis (MS) patients, suggesting a role in immune tolerance breakdown and disease pathogenesis.
Area of Science:
- Immunology
- Molecular Biology
- Genetics
Background:
- Multiple sclerosis (MS) pathogenesis involves immune system tolerance breakdown, but molecular mechanisms remain unclear.
- Long non-coding RNAs (lncRNAs) are implicated in regulating immunological pathways.
- Understanding novel lncRNAs like TOB1-AS1 is crucial for elucidating MS mechanisms.
Purpose of the Study:
- To evaluate the expression of the novel lncRNA TOB1-AS1 and its associated coding genes in the peripheral blood of MS patients.
- To investigate the role of TOB1-AS1 in maintaining immune tolerance in the context of MS.
- To assess the potential involvement of TOB1-AS1 dysregulation in MS pathogenesis.
Main Methods:
- Recruited 39 MS patients and 32 healthy controls.
- Quantified transcript levels of TOB1-AS1, TOB1, SKP2, and TSG using real-time PCR.
- Analyzed potential sex hormone receptor binding sites on target gene promoters via JASPR software.
Main Results:
- Demonstrated a negative correlation between TOB1-AS1 expression and the Expanded Disability Status Scale (EDSS) in MS patients.
- Observed significant dysregulation in the co-expression of TOB1-AS1 lncRNA and its coding genes in MS patients compared to controls.
- Identified potential sex hormone receptor binding sites on target gene promoters.
Conclusions:
- The dysregulation of TOB1-AS1 and its co-expressed coding genes may contribute to MS pathogenesis.
- Altered TOB1-AS1 expression could be linked to the breakdown of peripheral tolerance in MS.
- This pathway warrants further investigation for its role in MS and response to interferon treatment.
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