# Increased expression of complement C3c, iC3b, and cells containing CD11b or CD14 in experimentally induced psoriatic lesion

**Authors:** Dina Rahkola, Rauno J Harvima, Ilkka T Harvima

PMC · DOI: 10.1093/cei/uxae009 · 2024-02-04

## TL;DR

This study shows that psoriasis lesions triggered by skin trauma involve rapid and sustained increases in specific immune proteins and cells, especially in those with a positive Köbner reaction.

## Contribution

The study identifies distinct patterns of complement proteins and immune cell markers in psoriasis lesions based on the presence of the Köbner reaction.

## Key findings

- Positive Köbner reactions show rapid and sustained increases in epidermal C3c and iC3b and dermal C3c.
- CD11b+ and CD14+ cells correlate strongly in the early stages of the positive Köbner reaction and increase further over time.
- Differences in immune markers exist between Köbner-positive and -negative groups even before lesion induction.

## Abstract

Psoriasis is a chronic inflammatory skin disease with a characteristic isomorphic reaction, i.e. the Köbner reaction, induced by slight epidermal trauma. In this study, the tape-stripping technique was used to induce the development of Köbner reaction in 18 subjects with psoriasis. Eight subjects developed a positive reaction. To study the early cellular changes, skin biopsies were taken at the baseline and subsequent time points of 2 h, 1 d, 3 d, and 7 d for the immunostaining of complement C3c, iC3b, and cells expressing complement receptor 3 (CD11b/CD18; a receptor of iC3b) or CD14. The results show that the positive Köbner reaction is associated with rapid (2 h–1 d) and sustained (3–7 d) increase in the expression of epidermal C3c and iC3b and dermal C3c. In addition, there was a positive correlation between CD11b+ and CD14+ cells in baseline and 2 h–1 d biopsies with a subsequent increase in CD11b+ and CD14+ cells in 3–7 d biopsies in the Köbner-positive group. In the Köbner-negative group, only a transient increase in epidermal iC3b at 2 h–1 d, as well as rapid (2 h–1 d) and sustained increase (3–7 d) in dermal iC3b and CD14+ cells, was observed. In experiments with cultured monolayer keratinocytes, a slight cell damage already at 30 mJ/cm2 ultraviolet B irradiation led to increased expression of C3c, but not iC3b. Therefore, there are marked differences between Köbner groups in respect to the expression of C3c, iC3b, and cells expressing CD11b or CD14. Of note is the rapid and sustained increase in epidermal C3c and iC3b in the positive Köbner reaction.

The isomorphic psoriatic reaction is especially associated with rapid and sustained increase in the expression of epidermal C3c and iC3b and dermal C3c. In addition, the significant correlation between CD11b+ and CD14+ cells in 0 d and 2 h–1 d biopsies, as well as the subsequent increase in CD11b+ and CD14+ cells in 3–7 d biopsies, in the Köbner-positive group suggests that there are differences between Köbner groups in respect to dermal cellular environment already before the induction of the isomorphic psoriatic reaction. The expression of C3c immunoreactivity in cryosections from a representative Köbner-positive patient with psoriasis on day 0 (a), day 1 (b), and day 7 (c).The immunohistochemical staining of CD11b+ cells in cryosections from a Köbner-positive patient with psoriasis on day 0 (d) and day 7 (e).

Graphical Abstract

## Linked entities

- **Proteins:** C3C (C3c concentration), ITGAM (integrin subunit alpha M), CD14 (CD14 molecule)
- **Diseases:** psoriasis (MONDO:0005083)

## Full-text entities

- **Genes:** ITGAM (integrin subunit alpha M) [NCBI Gene 3684] {aka CD11B, CR3A, HNA-4, MAC-1, MAC1A, MO1A}, CD14 (CD14 molecule) [NCBI Gene 929], ITGB2 (integrin subunit beta 2) [NCBI Gene 3689] {aka CD18, LAD, LCAMB, LFA-1, MAC-1, MF17}
- **Diseases:** Kobner reaction (MESH:D016110), skin disease (MESH:D012871), trauma (MESH:D014947), psoriatic lesion (MESH:D015535), inflammatory (MESH:D007249), Psoriasis (MESH:D011565)
- **Chemicals:** ultraviolet B (-)

## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC11097906/full.md

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Source: https://tomesphere.com/paper/PMC11097906