Distribution of IL-31 and its receptor expressing cells in skin of atopic dermatitis

Abstract Background To understand the clinical segments of IL-31 signaling blockade therapy in pruritus of atopic dermatitis (AD), direct detection of the target proteins in the diseased tissues will provide crucial information. There is a lack of direct evidence concerning the cellular origin of IL...

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Published in:Journal of dermatological science 2014-06, Vol.74 (3), p.229-235
Main Authors: Kato, Atsuhiko, Fujii, Etsuko, Watanabe, Takeshi, Takashima, Yoshiaki, Matsushita, Hiroaki, Furuhashi, Takuya, Morita, Akimichi
Format: Article
Language:English
Subjects:
Atopic dermatitis
CD11b
Dermatitis, Atopic - metabolism
Dermatology
Dorsal root ganglia
Humans
IL-31
IL-31RA
Interleukins - metabolism
Nerve-fibers
Receptors, Interleukin - metabolism
Skin - metabolism
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Summary:Abstract Background To understand the clinical segments of IL-31 signaling blockade therapy in pruritus of atopic dermatitis (AD), direct detection of the target proteins in the diseased tissues will provide crucial information. There is a lack of direct evidence concerning the cellular origin of IL-31 in AD skins, and data on the expression of IL-31RA in AD are inconsistent. Also, there is no available information regarding IL-31RA protein expression in human dorsal root ganglia (DRG), which mediates the sensation of itch and is the long-suspected source of the protein. Objective We sought to obtain direct evidence concerning the distribution of IL-31- and IL-31RA-protein expressing cells and their characteristics in AD skin samples and in human DRG. Methods IL-31 was detected immunohistochemically in AD skins, and representative sections were double stained with IL-31 and several immune-markers. IL-31RA was stained immunohistochemically in AD skins and normal human DRG, and representative AD skins were double stained with IL-31RA and PGP9.5 (a nerve marker). Results IL-31-positive cells were observed as mononuclear infiltrating cells and as CD11b co-expressing cells in severe AD samples. As for IL-31RA, positive reactions were detected in keratinocytes and nerve fibers in the dermis of AD and in the neurons of normal DRG. Conclusion The detection of IL-31 in infiltrating cells of severe AD skin and of IL-31RA in nerve fibers of AD dermis and normal DRG indicates IL-31 signaling may be a contributing factor in the persistence and exacerbation of AD skin lesions.
ISSN:0923-1811
1873-569X
DOI:10.1016/j.jdermsci.2014.02.009