# The Role of Selected Proteins in the Pathogenesis of Psoriasis

**Authors:** Mateusz Matwiejuk, Agnieszka Kulczyńska-Przybik, Hanna Myśliwiec, Adrian Chabowski, Barbara Mroczko, Iwona Flisiak

PMC · DOI: 10.3390/ijms26136475 · International Journal of Molecular Sciences · 2025-07-04

## TL;DR

This review explores how specific proteins like elafin, chemerin, and NAMPT influence psoriasis by modulating inflammation and immune responses in the skin.

## Contribution

The paper introduces emerging proteins with dual pro- and anti-inflammatory roles as potential biomarkers or therapeutic targets in psoriasis.

## Key findings

- Elafin, chemerin, and NAMPT modulate inflammation and skin barrier function in psoriasis.
- These proteins interact within the immune–neuroendocrine network, contributing to the psoriatic microenvironment.
- They show potential as biomarkers or therapeutic targets due to their complex regulatory roles.

## Abstract

Psoriasis is a chronic, immune-mediated inflammatory skin disease with complex genetic, environmental, and immunological determinants. Beyond the skin, it affects multiple systems, including the joints and cardiovascular system. A hallmark of psoriasis is an overactivation of the innate and adaptive immune responses, leading to dysregulated cytokine signaling, altered keratinocyte function, and aberrant expression of structural and regulatory proteins. In recent years, growing attention has been given to the skin as a neuro–immuno–endocrine organ, with evidence showing the role of stress-related neuropeptides, UVB-induced immune modulation, and vitamin D signaling in the disease pathogenesis. This review highlights emerging evidence on key multifunctional proteins—elafin, chemerin, and NAMPT (visfatin)—that exert both pro- and anti-inflammatory actions. Although still underexplored, these molecules appear to contribute significantly to the psoriatic microenvironment by modulating inflammation, immunity, and skin barrier function. Their dual roles suggest complex interactions within the cutaneous immune–neuroendocrine network, positioning them as potential biomarkers or therapeutic targets in psoriasis. By integrating insights into classical and emerging mediators, this review aims to provide a comprehensive perspective on the evolving landscape of psoriasis pathophysiology.

## Linked entities

- **Proteins:** PI3 (peptidase inhibitor 3, skin-derived (SKALP)), RARRES2 (retinoic acid receptor responder (tazarotene induced) 2), NAMPT (nicotinamide phosphoribosyltransferase), NAMPT (nicotinamide phosphoribosyltransferase)
- **Diseases:** psoriasis (MONDO:0005083)

## Full-text entities

- **Genes:** NAMPT (nicotinamide phosphoribosyltransferase) [NCBI Gene 10135] {aka 1110035O14Rik, PBEF, PBEF1, VF, VISFATIN}, RARRES2 (retinoic acid receptor responder 2) [NCBI Gene 5919] {aka HP10433, TIG2}, PI3 (peptidase inhibitor 3) [NCBI Gene 5266] {aka ESI, SKALP, WAP3, WFDC14, cementoin}
- **Diseases:** Psoriasis (MESH:D011565), skin disease (MESH:D012871), inflammation (MESH:D007249), psoriatic (MESH:D015535)
- **Chemicals:** vitamin D (MESH:D014807)

## Full text

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## References

90 references — full list in the complete paper: https://tomesphere.com/paper/PMC12250344/full.md

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Source: https://tomesphere.com/paper/PMC12250344