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Hypothetical Atopic Dermatitis-Myeloproliferative Neoplasm Syndrome

Atopic dermatitis (AD) is a chronic inflammatory skin disease. Myeloproliferative neoplasms (MPNs) are hematopoietic malignancies caused by uncontrolled proliferation of hematopoietic stem/progenitor cells. Recent studies have described several mutant mice exhibiting both AD-like skin inflammation a...

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Autores principales: Kawakami, Toshiaki, Ando, Tomoaki, Kawakami, Yuko
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4547498/
https://www.ncbi.nlm.nih.gov/pubmed/26379670
http://dx.doi.org/10.3389/fimmu.2015.00434
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author Kawakami, Toshiaki
Ando, Tomoaki
Kawakami, Yuko
author_facet Kawakami, Toshiaki
Ando, Tomoaki
Kawakami, Yuko
author_sort Kawakami, Toshiaki
collection PubMed
description Atopic dermatitis (AD) is a chronic inflammatory skin disease. Myeloproliferative neoplasms (MPNs) are hematopoietic malignancies caused by uncontrolled proliferation of hematopoietic stem/progenitor cells. Recent studies have described several mutant mice exhibiting both AD-like skin inflammation and MPN. Common pathways for skin inflammation encompass overexpression of thymic stromal lymphopoietin and reduced signaling of epidermal growth factor receptor in the epidermis, while overproduction of granulocyte-colony-stimulating factor by keratinocytes and constitutive activation of Stat5 in hematopoietic stem cells are important for the development of MPN. The murine studies suggest the existence of a similar human disease tentatively termed as the atopic dermatitis-myeloproliferative neoplasm syndrome.
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spelling pubmed-45474982015-09-14 Hypothetical Atopic Dermatitis-Myeloproliferative Neoplasm Syndrome Kawakami, Toshiaki Ando, Tomoaki Kawakami, Yuko Front Immunol Immunology Atopic dermatitis (AD) is a chronic inflammatory skin disease. Myeloproliferative neoplasms (MPNs) are hematopoietic malignancies caused by uncontrolled proliferation of hematopoietic stem/progenitor cells. Recent studies have described several mutant mice exhibiting both AD-like skin inflammation and MPN. Common pathways for skin inflammation encompass overexpression of thymic stromal lymphopoietin and reduced signaling of epidermal growth factor receptor in the epidermis, while overproduction of granulocyte-colony-stimulating factor by keratinocytes and constitutive activation of Stat5 in hematopoietic stem cells are important for the development of MPN. The murine studies suggest the existence of a similar human disease tentatively termed as the atopic dermatitis-myeloproliferative neoplasm syndrome. Frontiers Media S.A. 2015-08-24 /pmc/articles/PMC4547498/ /pubmed/26379670 http://dx.doi.org/10.3389/fimmu.2015.00434 Text en Copyright © 2015 Kawakami, Ando and Kawakami. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Immunology
Kawakami, Toshiaki
Ando, Tomoaki
Kawakami, Yuko
Hypothetical Atopic Dermatitis-Myeloproliferative Neoplasm Syndrome
title Hypothetical Atopic Dermatitis-Myeloproliferative Neoplasm Syndrome
title_full Hypothetical Atopic Dermatitis-Myeloproliferative Neoplasm Syndrome
title_fullStr Hypothetical Atopic Dermatitis-Myeloproliferative Neoplasm Syndrome
title_full_unstemmed Hypothetical Atopic Dermatitis-Myeloproliferative Neoplasm Syndrome
title_short Hypothetical Atopic Dermatitis-Myeloproliferative Neoplasm Syndrome
title_sort hypothetical atopic dermatitis-myeloproliferative neoplasm syndrome
topic Immunology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4547498/
https://www.ncbi.nlm.nih.gov/pubmed/26379670
http://dx.doi.org/10.3389/fimmu.2015.00434
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