# Heat Shock Protein 70 Deficient Mice Exhibit Reduced Psoriasis-like Skin Inflammation

## TL;DR

Mice lacking HSP70 show less psoriasis-like skin inflammation, suggesting HSP70 plays a key role in the disease.

## Contribution

This study demonstrates that HSP70 deficiency reduces psoriasis-like inflammation in mice, offering a potential therapeutic target.

## Key findings

- Hsp70-deficient mice had reduced psoriasis-like inflammation and lower PASI scores.
- Hsp70 deficiency altered immune cell infiltration, with fewer LY6C+ monocytes and more LY6G+ neutrophils.
- HSP60 expression decreased while HSP90 expression increased in the absence of HSP70.

## Abstract

Background/Objectives: Psoriasis is a chronic, systemic, and multifactorial disease affecting approximately 1–2% of the Caucasian population. It is characterized by distinct histopathological features, including epidermal hyperplasia and infiltration of immune cells into the skin. Despite its high prevalence, the underlying mechanisms driving psoriasis remain incompletely understood. Heat shock proteins (HSPs), particularly HSP70, are known to play key roles in modulating immune responses and inflammation. Although previous studies have examined the involvement of HSPs in dermatological conditions such as psoriasis, current evidence remains inconclusive. In this study, we aimed to elucidate the role of Hsp70 deficiency in the pathogenesis of psoriasis using an in vivo model. Methods: We used male mice that were either genetically normal (Hsp70+/+) or lacked the Hsp70 gene (Hsp70−/−) at 8–12 weeks of age. Psoriasis was induced by applying imiquimod cream daily for 7 days. At the end of this period mice were sacrificed and blood and tissue collected for further analysis. The severity of the psoriasis was evaluated daily using the PASI Score. Results: Hsp70 depletion was accompanied by significantly decreased psoriatic-like skin inflammation, fewer histological abnormalities, and lower PASI scores. Flow cytometry analysis revealed a decrease in LY6C+ monocytes and an increase in LY6G+ neutrophils infiltration in Hsp70-deficient mice. In addition, HSP60 expression was lower in the absence of HSP70, while HSP90 expression was markedly elevated. Conclusions: These results point to a significant regulatory function of HSP70 in psoriatic inflammation and raise the possibility that it could be a therapeutic target.