Antimicrobial Peptide LL-37 Drives Rosacea Inflammation Through a Specific Immune Pathway | Research

The takeaway

LL-37 activates the Jak1/STAT1 pathway in skin cells to produce CXCL10, which recruits T-cells and drives rosacea-like inflammation.

Jak1/STAT1 → CXCL10 pathway
LL-37 drives T-cell-mediated rosacea inflammation through this signaling cascade

What the researchers found

LL-37 drives rosacea pathogenesis by activating Jak1/STAT1 signaling in keratinocytes, inducing CXCL10-mediated T-cell recruitment to the skin.

Why it matters

Identifying the specific signaling pathway from LL-37 to T-cell recruitment opens targeted therapeutic opportunities for rosacea, including Jak inhibitors.

How the study worked

Transcriptome profiling of LL-37-treated normal human keratinocytes, followed by pathway analysis identifying Jak1/STAT1 and CXCL10 as key mediators.

What this study cannot tell us

In vitro keratinocyte model — may not capture the full complexity of rosacea pathogenesis in intact skin with multiple cell types.

How to read the evidence

In vitro mechanistic study — strong for identifying molecular pathways but needs clinical validation of therapeutic implications.

When this study was published

Published 2026 in The Journal of Investigative Dermatology.

The bigger picture

This bridges innate and adaptive immunity in rosacea, suggesting that Jak inhibitors (already available for other skin conditions) could be repurposed for rosacea treatment.

Questions still open

Would Jak inhibitors (topical or oral) effectively treat rosacea?
Is CXCL10 a useful biomarker for rosacea severity or treatment response?

Common questions

What causes rosacea?

This study shows that overproduction of the antimicrobial peptide LL-37 in skin activates a specific immune pathway (Jak1/STAT1) that recruits inflammatory T-cells, causing the characteristic redness and inflammation.

Could this lead to new rosacea treatments?

Yes — Jak inhibitors, which block the pathway identified in this study, are already used for other skin conditions and could potentially be repurposed for rosacea.

Read the original research

Cathelicidin LL-37-Induced Transcriptome of Human Keratinocyte Identifies Chemokine CXCL10 Link to T-Cell-Mediated Rosacea Pathogenesis through Jak1/STAT1 Pathway.

The Journal of investigative dermatology, 146(3), 711-721.e6

View on PubMed ↗Publisher’s paper ↗

Citation

Ansari, Abdul W; Habib, Tanwir; Ahmad, Fareed; Raheed, Thesni; Elizabeth, Cynthia S; Al-Harami, Sara; Jochebeth, Anh; Steinhoff, Martin. (2026). Cathelicidin LL-37-Induced Transcriptome of Human Keratinocyte Identifies Chemokine CXCL10 Link to T-Cell-Mediated Rosacea Pathogenesis through Jak1/STAT1 Pathway.. The Journal of investigative dermatology, 146(3), 711-721.e6. https://doi.org/10.1016/j.jid.2025.08.003