Functional interleukin-33 receptors are expressed in early progenitor stages of allergy-related granulocytes

Hirofumi Tsuzuki, Yojiro Arinobu, Kohta Miyawaki, Ayako Takaki, Shun Ichiro Ota, Yuri Ota, Hiroki Mitoma, Mitsuteru Akahoshi, Yasuo Mori, Hiromi Iwasaki, Hiroaki Niiro, Hiroshi Tsukamoto, Koichi Akashi

研究成果: ジャーナルへの寄稿記事

9 引用 (Scopus)

抄録

Interleukin-33 (IL-33) induces T helper type 2 (Th2) cytokine production and eosinophilia independently of acquired immunity, leading to innate immunity-mediated allergic inflammation. Allergy-related innate myeloid cells such as eosinophils, basophils and mast cells express the IL-33 receptor (IL-33R), but it is still unknown how IL-33 regulates allergic inflammation involving these cells and their progenitors. Here, we revealed that the functional IL-33R was expressed on eosinophil progenitors (EoPs), basophil progenitors (BaPs) and mast cell progenitors (MCPs). In the presence of IL-33, these progenitors did not expand, but produced a high amount of Th2 and pro-inflammatory cytokines such as IL-9, IL-13, IL-1β and IL-6. The amount of cytokines produced by these progenitors was greater than that by mature cells. In vivo, IL-33 stimulated the expansion of EoPs, but it was dependent upon the elevated serum IL-5 that is presumably derived from type 2 innate lymphoid cells that express functional IL-33R. These data collectively suggest that EoPs, BaPs and MCPs are not only the sources of allergy-related granulocytes, but can also be sources of allergy-related cytokines in IL-33-induced inflammation. Because such progenitors can differentiate into mature granulocytes at the site of inflammation, they are potential therapeutic targets in IL-33-related allergic diseases.

元の言語英語
ページ(範囲)64-73
ページ数10
ジャーナルImmunology
150
発行部数1
DOI
出版物ステータス出版済み - 1 1 2017

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Granulocytes
Hypersensitivity
Eosinophils
Basophils
Mast Cells
Cytokines
Inflammation
Stem Cells
Interleukin-9
Interleukin-13
Interleukin-1 Receptor-Like 1 Protein
Interleukin-33
Interleukin-5
Eosinophilia
Adaptive Immunity
Myeloid Cells
Interleukin-1
Innate Immunity
Interleukin-6
Lymphocytes

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology

これを引用

Functional interleukin-33 receptors are expressed in early progenitor stages of allergy-related granulocytes. / Tsuzuki, Hirofumi; Arinobu, Yojiro; Miyawaki, Kohta; Takaki, Ayako; Ota, Shun Ichiro; Ota, Yuri; Mitoma, Hiroki; Akahoshi, Mitsuteru; Mori, Yasuo; Iwasaki, Hiromi; Niiro, Hiroaki; Tsukamoto, Hiroshi; Akashi, Koichi.

:: Immunology, 巻 150, 番号 1, 01.01.2017, p. 64-73.

研究成果: ジャーナルへの寄稿記事

Tsuzuki, Hirofumi ; Arinobu, Yojiro ; Miyawaki, Kohta ; Takaki, Ayako ; Ota, Shun Ichiro ; Ota, Yuri ; Mitoma, Hiroki ; Akahoshi, Mitsuteru ; Mori, Yasuo ; Iwasaki, Hiromi ; Niiro, Hiroaki ; Tsukamoto, Hiroshi ; Akashi, Koichi. / Functional interleukin-33 receptors are expressed in early progenitor stages of allergy-related granulocytes. :: Immunology. 2017 ; 巻 150, 番号 1. pp. 64-73.
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abstract = "Interleukin-33 (IL-33) induces T helper type 2 (Th2) cytokine production and eosinophilia independently of acquired immunity, leading to innate immunity-mediated allergic inflammation. Allergy-related innate myeloid cells such as eosinophils, basophils and mast cells express the IL-33 receptor (IL-33R), but it is still unknown how IL-33 regulates allergic inflammation involving these cells and their progenitors. Here, we revealed that the functional IL-33R was expressed on eosinophil progenitors (EoPs), basophil progenitors (BaPs) and mast cell progenitors (MCPs). In the presence of IL-33, these progenitors did not expand, but produced a high amount of Th2 and pro-inflammatory cytokines such as IL-9, IL-13, IL-1β and IL-6. The amount of cytokines produced by these progenitors was greater than that by mature cells. In vivo, IL-33 stimulated the expansion of EoPs, but it was dependent upon the elevated serum IL-5 that is presumably derived from type 2 innate lymphoid cells that express functional IL-33R. These data collectively suggest that EoPs, BaPs and MCPs are not only the sources of allergy-related granulocytes, but can also be sources of allergy-related cytokines in IL-33-induced inflammation. Because such progenitors can differentiate into mature granulocytes at the site of inflammation, they are potential therapeutic targets in IL-33-related allergic diseases.",
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AU - Tsuzuki, Hirofumi

AU - Arinobu, Yojiro

AU - Miyawaki, Kohta

AU - Takaki, Ayako

AU - Ota, Shun Ichiro

AU - Ota, Yuri

AU - Mitoma, Hiroki

AU - Akahoshi, Mitsuteru

AU - Mori, Yasuo

AU - Iwasaki, Hiromi

AU - Niiro, Hiroaki

AU - Tsukamoto, Hiroshi

AU - Akashi, Koichi

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AB - Interleukin-33 (IL-33) induces T helper type 2 (Th2) cytokine production and eosinophilia independently of acquired immunity, leading to innate immunity-mediated allergic inflammation. Allergy-related innate myeloid cells such as eosinophils, basophils and mast cells express the IL-33 receptor (IL-33R), but it is still unknown how IL-33 regulates allergic inflammation involving these cells and their progenitors. Here, we revealed that the functional IL-33R was expressed on eosinophil progenitors (EoPs), basophil progenitors (BaPs) and mast cell progenitors (MCPs). In the presence of IL-33, these progenitors did not expand, but produced a high amount of Th2 and pro-inflammatory cytokines such as IL-9, IL-13, IL-1β and IL-6. The amount of cytokines produced by these progenitors was greater than that by mature cells. In vivo, IL-33 stimulated the expansion of EoPs, but it was dependent upon the elevated serum IL-5 that is presumably derived from type 2 innate lymphoid cells that express functional IL-33R. These data collectively suggest that EoPs, BaPs and MCPs are not only the sources of allergy-related granulocytes, but can also be sources of allergy-related cytokines in IL-33-induced inflammation. Because such progenitors can differentiate into mature granulocytes at the site of inflammation, they are potential therapeutic targets in IL-33-related allergic diseases.

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