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Gene Expression Meta-Analysis of Potential Shared and Unique Pathways between Autoimmune Diseases under Anti-TNFα

Charalabos Antonatos1, Mariza Panoutsopoulou1, Georgios K Georgakilas1,2

  • 1Laboratory of Genetics, Section of Genetics, Cell Biology and Development, Department of Biology, University of Patras, 26504 Patras, Greece.

Genes
|May 28, 2022
PubMed

Insights

Anti-tumor necrosis factor (TNFα) therapy shows varied responses in autoimmune diseases like psoriasis (PsO), inflammatory bowel disease (IBD), and rheumatoid arthritis (RA). This meta-analysis reveals distinct gene expression patterns and common anti-inflammatory pathways, including IL-10 signaling, in response to anti-TNFα treatment.

Area of Science:

  • Immunology
  • Genomics
  • Computational Biology

Background:

  • Anti-tumor necrosis factor alpha (anti-TNFα) therapy is a cornerstone treatment for autoimmune diseases.
  • Patient responses to anti-TNFα therapy are highly variable, necessitating a deeper understanding of underlying mechanisms.
  • Psoriasis (PsO), inflammatory bowel disease (IBD), and rheumatoid arthritis (RA) are key autoimmune conditions where anti-TNFα efficacy is observed but patient heterogeneity exists.

Purpose of the Study:

  • To conduct a meta-analysis of gene expression data from patients with PsO, IBD, and RA treated with anti-TNFα therapy.
  • To identify differentially expressed genes (DEGs) and enriched pathways associated with treatment response across these diseases.
  • To explore common and disease-specific molecular mechanisms influenced by anti-TNFα therapy.

Main Methods:

  • Meta-analysis of publicly available gene expression cDNA microarray datasets for IBD, PsO, and RA.
  • Restricted maximum likelihood method for five disease-specific and one combined random-effects meta-analyses.
  • Gene Ontology and Reactome Pathway enrichment analyses, and STRING database for gene interaction analysis.

Main Results:

  • Identified distinct pro-inflammatory DEGs that were down-regulated in each disease-specific meta-analysis.
  • Pathway analyses revealed common inflammatory patterns contributing to the pathogenesis of IBD, PsO, and RA.
  • Combined meta-analyses highlighted DEGs involved in anti-inflammatory pathways, particularly Interleukin-10 (IL-10) signaling.

Conclusions:

  • This study provides a transcriptomic framework for understanding anti-TNFα therapy response in IBD, PsO, and RA.
  • The findings suggest that IL-10 signaling plays a crucial role in the anti-inflammatory effects of anti-TNFα therapy.
  • Further elucidation of these complex molecular interactions could identify novel therapeutic targets for these autoimmune diseases.
Keywords:
anti-TNFαautoimmunegene expressionmeta-analysispharmacogenomics

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