Heterogeneity of Treg/Th17 According to Cancer Progression and Modification in Biliary Tract Cancers via Self-Producing Cytokines.


Journal

Digestive diseases and sciences
ISSN: 1573-2568
Titre abrégé: Dig Dis Sci
Pays: United States
ID NLM: 7902782

Informations de publication

Date de publication:
10 2020
Historique:
received: 29 07 2019
accepted: 11 12 2019
pubmed: 20 12 2019
medline: 1 1 2021
entrez: 20 12 2019
Statut: ppublish

Résumé

We previously demonstrated that inflammatory cytokine interleukin-6 (IL-6) was produced during cancer progression, worked together with transforming growth factor-beta 1 (TGF-β1), and induced the epithelial-mesenchymal transition (EMT) with chemo-resistance against gemcitabine (GR) at the invasion front of biliary tract cancers (BTCs). However, the significance of cytokine-induced T cell accumulation at the tumor microenvironment in biliary tract cancer (BTC) is not well understood. Because these cytokines (IL-6 and TGF-β1) are able to differentiate naïve T cells into Foxp3-expressing T cells (Tregs) and/or IL-17-producing T helper 17 (Th17) cells, we investigated the relationship between heterogeneous, cancer-producing cytokines and T cell differentiation. In total, 127 curative resected specimens from patients with BTCs at Osaka University Hospital between 2000 and 2012 were evaluated for IL-6, TGF-β1, Tregs, and Th17 cells by immunohistochemistry. The ability of BTC-GR cells to undergo T cell differentiation was investigated in vitro. Tregs accumulated at the tumor center and Th17 cells accumulated at the invasion front during cancer progression and/or metastasis; each signaled poor prognosis. Treg accumulation was related to TGF-β1 expression by cancer cells, and Th17 cell accumulation was related to IL-6 expression by cancer cells, in resected specimens; this was confirmed in vitro. Compared with parent cells, GR cells produced IL-6 but not TGF-β1 in a time-dependent manner, had EMT features, and induced T cell differentiation to Th17 cells but not Tregs. Cytokines produced by cancer cells (IL-6 and TGF-β1) induced heterogeneity of Tregs and Th17 cells in the tumor microenvironment, supporting progression of BTC.

Sections du résumé

BACKGROUND/AIM
We previously demonstrated that inflammatory cytokine interleukin-6 (IL-6) was produced during cancer progression, worked together with transforming growth factor-beta 1 (TGF-β1), and induced the epithelial-mesenchymal transition (EMT) with chemo-resistance against gemcitabine (GR) at the invasion front of biliary tract cancers (BTCs). However, the significance of cytokine-induced T cell accumulation at the tumor microenvironment in biliary tract cancer (BTC) is not well understood. Because these cytokines (IL-6 and TGF-β1) are able to differentiate naïve T cells into Foxp3-expressing T cells (Tregs) and/or IL-17-producing T helper 17 (Th17) cells, we investigated the relationship between heterogeneous, cancer-producing cytokines and T cell differentiation.
METHODS
In total, 127 curative resected specimens from patients with BTCs at Osaka University Hospital between 2000 and 2012 were evaluated for IL-6, TGF-β1, Tregs, and Th17 cells by immunohistochemistry. The ability of BTC-GR cells to undergo T cell differentiation was investigated in vitro.
RESULTS
Tregs accumulated at the tumor center and Th17 cells accumulated at the invasion front during cancer progression and/or metastasis; each signaled poor prognosis. Treg accumulation was related to TGF-β1 expression by cancer cells, and Th17 cell accumulation was related to IL-6 expression by cancer cells, in resected specimens; this was confirmed in vitro. Compared with parent cells, GR cells produced IL-6 but not TGF-β1 in a time-dependent manner, had EMT features, and induced T cell differentiation to Th17 cells but not Tregs.
CONCLUSION
Cytokines produced by cancer cells (IL-6 and TGF-β1) induced heterogeneity of Tregs and Th17 cells in the tumor microenvironment, supporting progression of BTC.

Identifiants

pubmed: 31853779
doi: 10.1007/s10620-019-06011-9
pii: 10.1007/s10620-019-06011-9
doi:

Substances chimiques

Antimetabolites, Antineoplastic 0
Cytokines 0
FOXP3 protein, human 0
Forkhead Transcription Factors 0
IL6 protein, human 0
Interleukin-17 0
Interleukin-6 0
TGFB1 protein, human 0
Transforming Growth Factor beta1 0
Deoxycytidine 0W860991D6
Gemcitabine 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

2937-2948

Auteurs

Mitsuru Kinoshita (M)

Department of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, 2-2 (E2) Yamadaoka, Suita, 537-8511, Japan.

Shogo Kobayashi (S)

Department of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, 2-2 (E2) Yamadaoka, Suita, 537-8511, Japan.

Kunihito Gotoh (K)

Department of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, 2-2 (E2) Yamadaoka, Suita, 537-8511, Japan.

Masahiko Kubo (M)

Department of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, 2-2 (E2) Yamadaoka, Suita, 537-8511, Japan.

Koji Hayashi (K)

Department of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, 2-2 (E2) Yamadaoka, Suita, 537-8511, Japan.

Yoshifumi Iwagami (Y)

Department of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, 2-2 (E2) Yamadaoka, Suita, 537-8511, Japan.

Daisaku Yamada (D)

Department of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, 2-2 (E2) Yamadaoka, Suita, 537-8511, Japan.

Hirofumi Akita (H)

Department of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, 2-2 (E2) Yamadaoka, Suita, 537-8511, Japan.

Takehiro Noda (T)

Department of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, 2-2 (E2) Yamadaoka, Suita, 537-8511, Japan.

Tadafumi Asaoka (T)

Department of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, 2-2 (E2) Yamadaoka, Suita, 537-8511, Japan.

Yutaka Takeda (Y)

Department of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, 2-2 (E2) Yamadaoka, Suita, 537-8511, Japan.
Department of Surgery, Kansai Rosai Hospital, Amagasaki, Japan.

Masahiro Tanemura (M)

Department of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, 2-2 (E2) Yamadaoka, Suita, 537-8511, Japan.
Department of Surgery, Osaka Police Hospital, Osaka, Japan.

Hidetoshi Eguchi (H)

Department of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, 2-2 (E2) Yamadaoka, Suita, 537-8511, Japan. heguchi@gesurg.med.osaka-u.ac.jp.

Shinya Urakawa (S)

Department of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, 2-2 (E2) Yamadaoka, Suita, 537-8511, Japan.
Clinical Research in Tumor Immunology, Graduate School of Medicine, Osaka University, Suita, Japan.

Kumiko Goto (K)

Clinical Research in Tumor Immunology, Graduate School of Medicine, Osaka University, Suita, Japan.
Drug Discovery and Disease Research Laboratory, Shionogi & Co., Ltd., Toyonaka, Osaka, Japan.

Kayoko Maekawa (K)

Clinical Research in Tumor Immunology, Graduate School of Medicine, Osaka University, Suita, Japan.

Hisashi Wada (H)

Clinical Research in Tumor Immunology, Graduate School of Medicine, Osaka University, Suita, Japan.

Masaki Mori (M)

Department of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, 2-2 (E2) Yamadaoka, Suita, 537-8511, Japan.
Department of Surgery and Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.

Yuichiro Doki (Y)

Department of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, 2-2 (E2) Yamadaoka, Suita, 537-8511, Japan.

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