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Study breakdown

How LL-37 and Other Antimicrobial Peptides Bridge Innate and Adaptive Immunity in Psoriasis

ReviewModerate evidence
The takeaway

Antimicrobial peptides (LL-37, defensins, S100 proteins, lipocalin 2, RNase 7) are overexpressed in psoriatic skin and link innate and adaptive immune responses driving disease progression.

5 AMP classes

LL-37, β-defensins, S100 proteins, lipocalin 2, and RNase 7 all overexpressed and immunomodulatory in psoriasis

What the researchers found

LL-37, defensins, S100 proteins, lipocalin 2, and RNase 7 are highly expressed in psoriatic skin and bridge innate and adaptive immune responses in disease pathogenesis.

Why it matters

Understanding how AMPs drive psoriasis — rather than just defend against infection — could lead to targeted therapies that modulate specific AMP functions without compromising antimicrobial defense.

The numbers in context

LL-37, hBD1-4, S100 proteins, lipocalin 2, RNase 7 all highly expressed in psoriatic lesions

How the study worked

Narrative review of recent literature on AMPs in psoriasis, focusing on immunomodulatory mechanisms linking innate and adaptive immunity.

Who was studied

Review of literature on AMPs in psoriasis: LL-37, hBD1-4, S100 proteins, lipocalin 2, RNase 7

What this study cannot tell us

Narrative review — no systematic search methodology; mostly mechanistic data from in vitro and animal studies; clinical implications of AMP-targeting therapies largely speculative.

How to read the evidence

Moderate — well-supported review of established findings in psoriasis AMP biology.

When this study was published

Published in 2020; AMP roles in autoimmune skin disease continue to be refined.

The bigger picture

LL-37's role in psoriasis (activating dendritic cells via DNA complexes) was a landmark discovery. This review integrates newer findings showing that multiple AMP classes cooperate in driving psoriatic inflammation.

Questions still open

  • Could selectively blocking LL-37's immunomodulatory function (while preserving antimicrobial activity) treat psoriasis?
  • Which AMP is the most critical driver of psoriasis — LL-37, defensins, or S100 proteins?
  • Do AMP-targeting therapies risk increasing infection susceptibility?

Common questions

Why do protective peptides cause psoriasis?
In psoriasis, AMPs are overproduced and start activating immune cells beyond their antimicrobial role — forming complexes with DNA and activating dendritic cells that drive the inflammatory T cell response.
Is LL-37 the main culprit?
LL-37 was the first AMP linked to psoriasis (via DNA complexes activating dendritic cells), but this review shows defensins, S100 proteins, and others also play important bridging roles.

Read the original research

Antimicrobial peptides: bridging innate and adaptive immunity in the pathogenesis of psoriasis.

Chinese medical journal, 133(24), 2966-2975

Citation

Ma, Jing-Yi; Shao, Shuai; Wang, Gang. (2020). Antimicrobial peptides: bridging innate and adaptive immunity in the pathogenesis of psoriasis.. Chinese medical journal, 133(24), 2966-2975. https://doi.org/10.1097/CM9.0000000000001240