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Differential MicroRNA Expression in Chronic Spontaneous Urticaria in Relation to Treatment Response
Youngsoo Lee1, Jin Young Noh2,3,4, Jiwon Yoon5
1Department of Allergy and Clinical Immunology, Ajou University School of Medicine, Suwon, Korea.
Distinct serum microRNA (miRNA) signatures correlate with treatment responses in chronic spontaneous urticaria (CSU). MiR-93-5p and its targets like CCND1 are implicated in both antihistamine refractoriness and omalizumab effectiveness, guiding personalized CSU therapy.
Area of Science:
- Immunology
- Dermatology
- Genetics
Background:
- Chronic spontaneous urticaria (CSU) is a mast cell-driven skin disorder with complex immune dysregulation.
- MicroRNAs (miRNAs) are key post-transcriptional regulators implicated in various diseases, including CSU.
- Understanding miRNA roles in CSU pathogenesis and treatment response is crucial for therapeutic advancements.
Purpose of the Study:
- To investigate differentially expressed serum miRNAs in CSU patients.
- To identify serum miRNA signatures associated with treatment response to H₁-antihistamines (H1AHs) and omalizumab.
- To explore the potential mechanistic links between miRNAs and CSU treatment outcomes.
Main Methods:
- Serum samples from 30 CSU patients and 10 healthy controls were analyzed.
- Serum miRNA profiling was performed using the Affymetrix GeneChip® miRNA 4.0 Array.
- Bioinformatic analyses were conducted to identify differentially expressed miRNAs, predict target genes, and assess pathway enrichment.
Main Results:
- Eighteen miRNAs were differentially expressed between CSU patients and controls (10 upregulated, 8 downregulated).
- Twenty-three miRNAs were downregulated in H1AH nonresponders compared to responders.
- Four miRNAs (hsa-miR-503-5p, hsa-miR-1282, hsa-miR-93-5p, hsa-miR-638) were reduced in complete responders to omalizumab.
- hsa-miR-93-5p and its target CCND1 were associated with both H1AH nonresponsiveness and omalizumab response.
Conclusions:
- Distinct serum miRNA profiles are associated with treatment responses in CSU.
- MiR-93-5p, with network targets including MYC, CCND1, and HSPA8, highlights shared pathways in H1AH refractoriness and omalizumab responsiveness.
- These findings provide mechanistic insights into CSU pathogenesis and support personalized treatment strategies.
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