TY - JOUR
T1 - Immunomodulation by inflammation during liver and gastrointestinal tumorigenesis and aging
AU - Nagai, Nao
AU - Kudo, Yotaro
AU - Aki, Daisuke
AU - Nakagawa, Hayato
AU - Taniguchi, Koji
N1 - Funding Information:
Funding: This work is supported by JSPS KAKENHI (JP 15K21775, JP 20H03758), AMED (PRIME) under Grant Number JP 18gm6210008/19gm6210008/20gm6210008, the “Kibou Projects” Startup Support for Young Researchers in Immunology, the Keio Gijuku Academic Development Funds, the Uehara Memorial Foundation, the Kanae Foundation for the Promotion of Medical Science, the Astellas Foundation for Research on Metabolic Disorders, the SENSHIN Medical Research Foundation, research grants from Bristol-Myers Squibb, the SGH foundation, the MSD Life Science Foundation, the Ichiro Kanehara Foundation for the Promotion of Medical Sciences and Medical Care, the Yasuda Medical Foundation, the Suzuken Memorial Foundation, the Pancreas Research Foundation of Japan, the Waksman Foundation of Japan Inc., the Japanese Foundation for Multidisciplinary Treatment of Cancer, Project Mirai Cancer Research Grants from the Japan Cancer Society, the Okinaka Memorial Institute for Medical Research, the Asahi Glass Foundation, the Foundation for Promotion of Cancer Research, the Kobayashi Foundation for Cancer Research, the Toray Science Foundation, the Vehicle Racing Commemorative Foundation, the JSR-Keio University Medical and Chemical Innovation Center (JKiC), a research grant from the Public Trust Surgery Research Fund, a Research Grant of the Princess Takamatsu Cancer Research Fund, the Tokyo Biomedical Foundation, the Daiichi Sankyo Foundation of Life Science, the Mochida Memorial Foundation for Medical and Pharmaceutical Research, the Medical Research Encouragement Prize of the Japan Medical Association, the Terumo Foundation for Life Sciences and Arts, the Ya-kult-Bioscience Foundation, the Novartis Foundation, the Mitsubishi Foundation, and the Takeda Science Foundation (all to K.T.). This work is also supported by Bristol-Myers Squibb Research Grant, Takeda Science Foundation, MSD Life Science Foundation, The Naito Foundation, Life Science Foundation of Japan, The Cell Science Research Foundation, KAKENHI Grant Number 18K07994, AMED under Grant Number JP19fk0210059, JP20fk0210059, JP18fk0210040, JP19fk0210040, and JP20fk0210040 (all to H.N.).
Funding Information:
This work is supported by JSPS KAKENHI (JP 15K21775, JP 20H03758), AMED (PRIME) under Grant Number JP 18gm6210008/19gm6210008/20gm6210008, the “Kibou Projects” Startup Support for Young Researchers in Immunology, the Keio Gijuku Academic Development Funds, the Uehara Memorial Foundation, the Kanae Foundation for the Promotion of Medical Science, the Astellas Foundation for Research on Metabolic Disorders, the SENSHIN Medical Research Foundation, research grants from Bristol-Myers Squibb, the SGH foundation, the MSD Life Science Foundation, the Ichiro Kanehara Foundation for the Promotion of Medical Sciences and Medical Care, the Yasuda Medical Foundation, the Suzuken Memorial Foundation, the Pancreas Research Foundation of Japan, the Waksman Foundation of Japan Inc., the Japanese Foundation for Multidisciplinary Treatment of Cancer, Project Mirai Cancer Research Grants from the Japan Cancer Society, the Okinaka Memorial Institute for Medical Research, the Asahi Glass Foundation, the Foundation for Promotion of Cancer Research, the Kobayashi Foundation for Cancer Research, the Toray Science Foundation, the Vehicle Racing Commemorative Foundation, the JSR-Keio University Medical and Chemical Innovation Center (JKiC), a research grant from the Public Trust Surgery Research Fund, a Research Grant of the Princess Takamatsu Cancer Research Fund, the Tokyo Biomedical Foundation, the Daiichi Sankyo Foundation of Life Science, the Mochida Memorial Foundation for Medical and Pharmaceutical Research, the Medical Research Encouragement Prize of the Japan Medical Association, the Terumo Foundation for Life Sciences and Arts, the Yakult-Bioscience Foundation, the Novartis Foundation, the Mitsubishi Foundation, and the Takeda Science Foundation (all to K.T.). This work is also supported by Bristol-Myers Squibb Research Grant, Takeda Science Foundation, MSD Life Science Foundation, The Naito Foundation, Life Science Foundation of Japan, The Cell Science Research Foundation, KAKENHI Grant Number 18K07994, AMED under Grant Number JP19fk0210059, JP20fk0210059, JP18fk0210040, JP19fk0210040, and JP20fk0210040 (all to H.N.).
Publisher Copyright:
© 2021 by the authors. Licensee MDPI, Basel, Switzerland.
PY - 2021/3/1
Y1 - 2021/3/1
N2 - Chronic inflammation is thought to promote tumorigenesis and metastasis by several mechanisms, such as affecting tumor cells directly, establishing a tumor-supporting microenvironment, enhancing tumor angiogenesis, and suppressing antitumor immunity. In this review, we discuss the recent advances in our understanding of how inflammation induces the immunosuppressive tumor microenvironment, such as increasing the level of pro-inflammatory cytokines, chemokines, and immunosuppressive molecules, inducing immune checkpoint molecules and cytotoxic T-cell exhaustion, and accumulating regulatory T (Treg) cells and myeloid-derived suppressor cells (MDSCs). The suppression of antitumor immunity by inflammation is especially examined in the liver and colorectal cancer. In addition, chronic inflammation is induced during aging and causes age-related diseases, including cancer, by affecting immunity. Therefore, we also discuss the age-related diseases regulated by inflammation, especially in the liver and colon.
AB - Chronic inflammation is thought to promote tumorigenesis and metastasis by several mechanisms, such as affecting tumor cells directly, establishing a tumor-supporting microenvironment, enhancing tumor angiogenesis, and suppressing antitumor immunity. In this review, we discuss the recent advances in our understanding of how inflammation induces the immunosuppressive tumor microenvironment, such as increasing the level of pro-inflammatory cytokines, chemokines, and immunosuppressive molecules, inducing immune checkpoint molecules and cytotoxic T-cell exhaustion, and accumulating regulatory T (Treg) cells and myeloid-derived suppressor cells (MDSCs). The suppression of antitumor immunity by inflammation is especially examined in the liver and colorectal cancer. In addition, chronic inflammation is induced during aging and causes age-related diseases, including cancer, by affecting immunity. Therefore, we also discuss the age-related diseases regulated by inflammation, especially in the liver and colon.
KW - Aging
KW - Cancer
KW - Immunosuppression
KW - Inflammation
KW - Tumor microenvironment
UR - http://www.scopus.com/inward/record.url?scp=85101231004&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85101231004&partnerID=8YFLogxK
U2 - 10.3390/ijms22052238
DO - 10.3390/ijms22052238
M3 - Review article
C2 - 33668122
AN - SCOPUS:85101231004
SN - 1661-6596
VL - 22
SP - 1
EP - 15
JO - International Journal of Molecular Sciences
JF - International Journal of Molecular Sciences
IS - 5
M1 - 2238
ER -
