Content » Vol 100, November

Investigative Report

Protein and mRNA Expression Levels of Interleukin-17A, -17F and -22 in Blood and Skin Samples of Patients with Mycosis Fungoides

Despoina Papathemeli, Aikaterini Patsatsi, Dimitrios Papanastassiou, Triantafyllia Koletsa, Thomas Papathemelis, Chrysostomos Avgeros, Olga Pikou, Elizabeth Lazaridou, Elisavet Georgiou
DOI: 10.2340/00015555-3688

Abstract

This study investigated the expression of interleukin (IL)-17A, -17F and -22 in mycosis fungoides. Blood samples were collected from 50 patients with mycosis fungoides and 50 healthy controls. Skin samples were obtained from 26 patients with mycosis fungoides and 5 healthy controls. Protein levels of IL-17A, -17F and -22 were measured in serum by multiplex enzyme-linked immunosorbent assay, and mRNA expression levels were measured in blood and skin samples by real-time quantitative reverse transcription PCR. Both IL-17A and IL-17F mRNA expression levels were significantly lower in blood of patients with mycosis fungoides in comparison with healthy controls. IL-22 serum levels and expression levels of IL-22 mRNA in skin tissue, were significantly increased in patients with mycosis fungoides in comparison with healthy controls. These results suggest that low levels of IL-17A and IL-17F in mycosis fungoides may be connected to impaired immune surveillance contributing to tumourigenesis. Upregulation of IL-22 may play a role in the establishment of the tumour microenvironment in mycosis fungoides.

Significance

The role of interleukin-17A, -17F and -22 in many inflammatory and autoimmune diseases, including psoriasis, is well established. Little is known, however, about the role of these cytokines in mycosis fungoides. This study investigated the expression levels of interleukin-17A, -17F and -22 in blood and lesional skin samples of patients with mycosis fungoides in comparison with healthy controls. The results suggest that the mycosis fungoides tumour microenvironment is characterized by downregulation of interleukin-17A and -17F and upregulation of interleukin-22.

Supplementary content

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