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タイトル: C10orf99/GPR15L Regulates Proinflammatory Response of Keratinocytes and Barrier Formation of the Skin
著者: Dainichi, Teruki
Nakano, Yuri
Doi, Hiromi
Nakamizo, Satoshi  kyouindb  KAKEN_id  orcid https://orcid.org/0000-0001-9332-0369 (unconfirmed)
Nakajima, Saeko  kyouindb  KAKEN_id  orcid https://orcid.org/0000-0003-0831-1447 (unconfirmed)
Matsumoto, Reiko
Farkas, Thomas
Wong, Pui Mun
Narang, Vipin
Moreno Traspas, Ricardo
Kawakami, Eiryo
Guttman-Yassky, Emma
Dreesen, Oliver
Litman, Thomas
Reversade, Bruno
Kabashima, Kenji  kyouindb  KAKEN_id  orcid https://orcid.org/0000-0002-0773-0554 (unconfirmed)
著者名の別形: 大日, 輝記
仲野, 祐里
土居, 博美
中溝, 聡
中島, 沙恵子
松本, 玲子
川上, 英良
椛島, 健治
キーワード: EIME
keratinocyte
GPR15L
C10orf99
2610528A11Rik
atopic dermatitis
psoriasis
発行日: 2022
出版者: Frontiers Media SA
誌名: Frontiers in Immunology
巻: 13
論文番号: 825032
抄録: The epidermis, outermost layer of the skin, forms a barrier and is involved in innate and adaptive immunity in an organism. Keratinocytes participate in all these three protective processes. However, a regulator of keratinocyte protective responses against external dangers and stresses remains elusive. We found that upregulation of the orphan gene 2610528A11Rik was a common factor in the skin of mice with several types of inflammation. In the human epidermis, peptide expression of G protein-coupled receptor 15 ligand (GPR15L), encoded by the human ortholog C10orf99, was highly induced in the lesional skin of patients with atopic dermatitis or psoriasis. C10orf99 gene transfection into normal human epidermal keratinocytes (NHEKs) induced the expression of inflammatory mediators and reduced the expression of barrier-related genes. Gene ontology analyses showed its association with translation, mitogen-activated protein kinase (MAPK), mitochondria, and lipid metabolism. Treatment with GPR15L reduced the expression levels of filaggrin and loricrin in human keratinocyte 3D cultures. Instead, their expression levels in mouse primary cultured keratinocytes did not show significant differences between the wild-type and 2610528A11Rik deficient keratinocytes. Lipopolysaccharide-induced expression of Il1b and Il6 was less in 2610528A11Rik deficient mouse keratinocytes than in wild-type, and imiquimod-induced psoriatic dermatitis was blunted in 2610528A11Rik deficient mice. Furthermore, repetitive subcutaneous injection of GPR15L in mouse ears induced skin inflammation in a dose-dependent manner. These results suggest that C10orf99/GPR15L is a primary inducible regulator that reduces the barrier formation and induces the inflammatory response of keratinocytes.
記述: 皮膚表面で産生されるペプチドのはたらきを発見 --アトピー性皮膚炎、乾癬でも--. 京都大学プレスリリース. 2022-02-22.
著作権等: © 2022 Dainichi, Nakano, Doi, Nakamizo, Nakajima, Matsumoto, Farkas, Wong, Narang, Moreno Traspas, Kawakami, Guttman-Yassky, Dreesen, Litman, Reversade and Kabashima.
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) and the copyright owner(s) 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.
URI: http://hdl.handle.net/2433/268045
DOI(出版社版): 10.3389/fimmu.2022.825032
PubMed ID: 35273606
関連リンク: https://www.kyoto-u.ac.jp/ja/research-news/2022-02-22-0
出現コレクション:学術雑誌掲載論文等

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