Antimicrobial peptide LL-37 modulates immune cell chemokine secretion and skin-homing in psoriasis | Research

The takeaway

LL-37 significantly modulates chemokine secretion from PBMCs in Th1/Th17 inflammatory conditions, while psoriasis patients show altered T cell skin-homing marker expression including increased CCR6 and decreased CXCR3.

LL-37 reshapes chemokine landscape
The antimicrobial peptide LL-37 remarkably modulated immune cell chemokine secretion in psoriasis-mimicking conditions, potentially driving disease-associated immune cell skin homing

What the researchers found

Psoriatic T cells: increased CCR6, decreased CXCR3-high. Chemokine receptors varied by CLA/CD103 expression. LL-37 modulated chemokine secretion in Th1 and Th17 microenvironments. Th1 and Th17 stimulation produced distinct chemokine secretion clusters by PCA.

Why it matters

LL-37 is both a potential psoriasis trigger and autoantigen. Understanding how it modulates immune cell migration to the skin could reveal new therapeutic targets for controlling psoriatic inflammation.

How the study worked

Flow cytometry for T cell chemokine receptor and skin-homing marker expression (CLA, CD103, CCR6, CXCR3, CCR4). PBMC stimulation in Th1/Th17 mimicking conditions ± LL-37. Chemokine secretion profiling.

What this study cannot tell us

In vitro PBMC stimulation may not fully represent skin microenvironment. Observational comparison between psoriasis patients and controls. Specific chemokine effects of LL-37 need functional validation in skin models.

How to read the evidence

Translational study combining patient immunophenotyping with in vitro functional assays. Good mechanistic evidence for LL-37's immunomodulatory role.

When this study was published

Published in 2025.

The bigger picture

LL-37 is emerging as a key player in autoimmune skin disease, acting as both an immune modulator and potential autoantigen. This study reveals its ability to shape the chemokine landscape that drives immune cell recruitment to psoriatic skin.

Questions still open

Could anti-LL-37 therapy reduce psoriatic immune cell skin homing?
Does LL-37 modulation of chemokines contribute to psoriasis flares?
Are LL-37 levels in skin a predictor of psoriasis severity?

Common questions

What role does LL-37 play in psoriasis?

LL-37 is an antimicrobial peptide found at high levels in psoriatic skin. This study shows it modulates which chemokines (chemical signals) immune cells produce, potentially controlling which immune cells migrate to the skin and causing the inflammation seen in psoriasis. It may act as both a trigger and autoantigen in the disease.

Could targeting LL-37 help treat psoriasis?

Potentially. By reshaping the chemokine signals that recruit inflammatory immune cells to the skin, LL-37 appears to be a key driver of psoriatic inflammation. Therapies that block LL-37 or its downstream chemokine effects could reduce immune cell skin infiltration and disease severity.

Read the original research

Skin-Homing Potential of Peripheral Immune Cells From Psoriasis Patients and the Effects of LL-37 on Their Secretion of Chemokines During Psoriasis-Mimicking Stimulation.

Scandinavian journal of immunology, 102(5), e70066

View on PubMed ↗Publisher’s paper ↗

Citation

Sigurgrímsdóttir, Hildur; Eysteinsdóttir, Jenna Huld; Kristjánsson, Árni Kjalar; Agnarsson, Bjarni A; Freysdottir, Jona; Lúðvíksson, Björn Rúnar. (2025). Skin-Homing Potential of Peripheral Immune Cells From Psoriasis Patients and the Effects of LL-37 on Their Secretion of Chemokines During Psoriasis-Mimicking Stimulation.. Scandinavian journal of immunology, 102(5), e70066. https://doi.org/10.1111/sji.70066