Yukiko Ito MD, Sayaka Shibata MD, PhD, Asumi Koyama MD, Lixin Li MD, Eiki Sugimoto MD, Haruka Taira MD, Yuka Mizuno MD, Kentaro Awaji MD, PhD, Shinichi Sato MD, PhD
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Abstract
Background
Psoriasis is a chronic skin inflammatory disease characterized by epidermal proliferation and inflammatory cell infiltration. AXL is a tyrosine kinase receptor that promotes cell proliferation and invasion in cancer cells, and its expression is elevated in multiple tumors. However, less is known about its expression and function in inflammatory diseases.
Objectives
The aim of this study is to examine AXL expression in psoriasis and investigate the biological function of AXL under psoriatic conditions.
Results
AXL mRNA expression was decreased in psoriatic skin compared to healthy skin, and an inverse correlation with neutrophil-to-lymphocyte ratio and platelet-to-lymphocyte ratio was observed. Immunohistochemical staining of psoriatic skin revealed decreased AXL expression of the epidermis and an increased number of AXL-positive dendritic cells in the dermis. Stimulation of epidermal keratinocytes with antimicrobial peptide LL37, but not with IL-17A, resulted in decreased AXL expression. Knockdown of AXL in epidermal keratinocytes did not affect cell proliferation or expression of psoriasis-associated cytokines and chemokines.
Conclusion
Decreased epidermal AXL expression and increased infiltration of AXL-expressing dendritic cells were revealed in psoriasis.
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