Omics · study · 2026
Neutralizing IL-22RA1 improves histological and molecular alterations associated with atopic dermatitis pathogenesis
Listed in NCBI GEO
BACKGROUND: A subgroup of patients with atopic dermatitis (AD) do not show sufficient improvement with current systemic therapies, highlighting the heterogeneity of the chronic inflammatory skin disease and the need for novel treatments.
Description
OBJECTIVES: In this study, we investigated the pathogenic contribution of the IL-22/IL-22 receptor (IL-22RA1) axis to AD skin inflammation in in vitro, ex vivo, and in vivo models to evaluate the therapeutic potential of blocking this axis.
METHODS: IL-22RA1 expression in AD skin was assessed by in situ hybridization. Inhibition of the IL-22/IL-22R signaling cascade was evaluated in a human AD in vitro model (3D skin equivalents) and a TPA mouse model using temtokibart, a humanized antibody directed against IL-22RA1. RESULTS: IL22RA1 was highly expressed in the epidermis of lesional AD skin versus non-lesional control skin; expression correlated positively with epidermal thickness and negatively with the barrier integrity marker loricrin.
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IL-22 stimulation in 3D skin equivalents induced a specific molecular signature associated with lack of terminal differentiation, altered lipid metabolism, and increased immune response. Inhibition of IL-22RA1 with temtokibart showed significant improvements in skin barrier integrity at the histological and molecular levels. IL-22RA1 inhibition in a skin inflammation mouse model with Zymo, a surrogate murine anti-IL-22RA1 monoclonal antibody for temtokibart, reduced local expression of Cxcl1 and S100a9.
CONCLUSIONS: These findings suggest that the IL-22/IL-22RA1 axis functionally contributes to AD pathogenesis. Thus, blocking IL-22RA1 represents a potentially valuable new therapeutic option.
Links
Get the data
- GEO FTP directory ftp.ncbi.nlm.nih.gov/geo/series/GSE313nnn/GSE313454 ↗
download · from NCBI GEO
Where it is published
- GEO accession page ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE313454 ↗
landing page · from NCBI GEO
Documentation and papers
- PRJNA1379549 ncbi.nlm.nih.gov/bioproject/PRJNA1379549 ↗
project · from NCBI GEO
Topics
- Stated by source
- Expression profiling by high throughput sequencing · Homo sapiens
- From keywords
- Life Sciences
- Inferred from text
- Disease 75%
Provenance · 1 source records, 8 field assertions
| Source | Key | Last seen | Raw |
|---|---|---|---|
| NCBI GEO | GSE313454 | 14 d ago | JSON v1 |
| Field | Assertion | Extractor | Evidence |
|---|---|---|---|
| access_level | source · NCBI GEO | connector:ncbi_geo@1.0.0 | |
| concepts[disease].local:disease:disease | enrichment · NCBI GEO | keyword-concept-rules@1.0.0 | title+description (75%) |
| concepts[field].local:field:life-sciences | mapping · NCBI GEO | connector:ncbi_geo@1.0.0 | |
| concepts[method].geo_series_type:expression-profiling-by-high-throughput-sequencing | source · NCBI GEO | connector:ncbi_geo@1.0.0 | /gdstype |
| concepts[organism].NCBITaxon:9606 | source · NCBI GEO | connector:ncbi_geo@1.0.0 | /taxon |
| description | source · NCBI GEO | connector:ncbi_geo@1.0.0 | /summary |
| publication_date | source · NCBI GEO | connector:ncbi_geo@1.0.0 | |
| title | source · NCBI GEO | connector:ncbi_geo@1.0.0 | /title |