# MicroRNAs—Are They Possible Markers of Allergic Diseases and Efficient Immunotherapy?

**Authors:** Krzysztof Specjalski, Marek Niedoszytko

PMC · DOI: 10.3390/ijms27020902 · 2026-01-16

## TL;DR

This paper explores the potential of microRNAs as non-invasive biomarkers for diagnosing and monitoring allergic diseases and immunotherapy.

## Contribution

The paper highlights miRNAs as novel candidates for biomarkers and therapeutic targets in allergic diseases.

## Key findings

- Certain miRNAs are associated with allergic rhinitis, asthma, and atopic dermatitis.
- miRNA profiles change during allergen immunotherapy, suggesting their role in immune tolerance.
- miRNAs may serve as therapeutic agents, but challenges in delivery and safety remain.

## Abstract

Micro-RNAs (miRNAs) are short, non-coding RNA molecules regulating genes’ expression. Studies published over last years demonstrated that they play an important role in allergic diseases by regulating humoral and cellular immunity, cytokine secretion and epithelium function. Some of them seem potential non-invasive biomarkers facilitating diagnosis of the most common allergic diseases, such as allergic rhinitis (miR-21, miR-126, miR-142-3p, miR-181a, miR-221), asthma (miR-16, miR-21, miR-126, miR-146a, miR-148a, miR-221, miR-223) and atopic dermatitis (miR-24, miR-124, miR-155, miR-191, miR-223, miR-483-5p), or objectively assessing severity of inflammation and endotype of the disease. In spite of the large body of literature available, its scientific value is limited due to the small numbers of study participants, heterogeneity of populations enrolled, and diverse methodology. Some studies have revealed significant changes in miRNAs’ profile in the course of allergen immunotherapy. Tolerance induction is associated with processes controlled by miRNAs: enhanced activity of Treg cells and increased production of tolerogenic IL-10 and TGF-β. Thus, miRNAs may be candidates as biomarkers of successful immunotherapy. Finally, they are also possible therapeutic agents or targets of therapies based on antagomirs blocking their activity. However, so far no studies are available that demonstrate efficacy in overcoming delivery barriers, tissue targeting or drugs’ safety. As a consequence, despite promising results of in vitro and animal model studies, translation into human therapeutic agents is uncertain.

## Linked entities

- **Proteins:** IL10 (interleukin 10), TGFB1 (transforming growth factor beta 1), treG (TreG)
- **Diseases:** allergic rhinitis (MONDO:0011786), asthma (MONDO:0004979), atopic dermatitis (MONDO:0004980)

## Full-text entities

- **Genes:** TGFB1 (transforming growth factor beta 1) [NCBI Gene 7040] {aka CAEND1, CED, DPD1, IBDIMDE, LAP, TGF-beta1}, MIR148A (microRNA 148a) [NCBI Gene 406940] {aka MIRN148, MIRN148A, hsa-mir-148, mir-148a}, MIR21 (microRNA 21) [NCBI Gene 406991] {aka MIRN21, hsa-mir-21, miR-21, miRNA21}, IL10 (interleukin 10) [NCBI Gene 3586] {aka CSIF, GVHDS, IL-10, IL10A, TGIF}, MIR146A (microRNA 146a) [NCBI Gene 406938] {aka MIRN146, MIRN146A, miR-146a, miRNA146A}, MIR221 (microRNA 221) [NCBI Gene 407006] {aka MIRN221, miRNA221, mir-221}, GDE1 (glycerophosphodiester phosphodiesterase 1) [NCBI Gene 51573] {aka 363E6.2, MIR16}, MIR191 (microRNA 191) [NCBI Gene 406966] {aka MIRN191, miR-191}, MIR223 (microRNA 223) [NCBI Gene 407008] {aka MIRN223, miRNA223, mir-223}, MIR155 (microRNA 155) [NCBI Gene 406947] {aka MIRN155, miRNA155, mir-155}, MIR126 (microRNA 126) [NCBI Gene 406913] {aka MIRN126, miRNA126, mir-126}
- **Diseases:** asthma (MESH:D001249), inflammation (MESH:D007249), Allergic Diseases (MESH:D004342), atopic dermatitis (MESH:D003876), allergic rhinitis (MESH:D065631)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

1 figure with captions in the complete paper: https://tomesphere.com/paper/PMC12841210/full.md

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Source: https://tomesphere.com/paper/PMC12841210