Interaction between gut microbiota and T cell immunity in colorectal cancer

This review delves into the complex and multi-layered mechanisms that govern the interaction between gut microbiota and T cells in the context of colorectal cancer (CRC), revealing a novel “microbiota-immune regulatory landscape” within the tumor microenvironment. As CRC progresses, the gut microbio...

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Published inAutoimmunity reviews Vol. 24; no. 6; p. 103807
Main Authors Jing, Zhuang, Yinhang, Wu, Jian, Chu, Zhanbo, Qu, Xinyue, Wu, Shuwen, Han
Format Journal Article
LanguageEnglish
Published Netherlands Elsevier B.V 30.05.2025
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IPA
TAM
HFD
TRM
MLN
Tfh
Th1
QS
IL
DSS
QX
EM
HCC
AM
LGG
CRC
TCM
SND
IBD
CC4
KD
SRY
GC
AOM
Fn
ID2
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Abstract This review delves into the complex and multi-layered mechanisms that govern the interaction between gut microbiota and T cells in the context of colorectal cancer (CRC), revealing a novel “microbiota-immune regulatory landscape” within the tumor microenvironment. As CRC progresses, the gut microbiota experiences a significant transformation in both its composition and metabolic patterns. On one hand, specific microbial entities within the gut microbiota can directly engage with T cells, functioning as “immunological triggers” that shape T-cell behavior. Simultaneously, microbial metabolites, such as short-chain fatty acids and bile acids, serve as “molecular regulators” that intricately govern T-cell function and differentiation, fine-tuning the immune response. On the other hand, the quorum-sensing mechanism, a recently recognized communication network among bacteria, also plays a pivotal role in orchestrating T-cell immunity. Additionally, the gut microbiota forms an intriguing connection with the neuro-immune regulatory axis, a largely unexplored “territory” in CRC research. Regarding treatment strategies, a diverse array of intervention approaches—including dietary modifications, the utilization of probiotics, bacteriophages, and targeted antibiotic therapies—offer promising prospects for restoring the equilibrium of the gut microbiota, thereby acting as “ecosystem renovators” that impede tumor initiation and progression. Nevertheless, the current research landscape in this field is fraught with challenges. These include significant variations in microbial composition, dietary preferences, and tumor microenvironments among individuals, a lack of large-scale cohort studies, and insufficient research that integrates tumor mutation analysis, gut microbiota investigations, and immune microenvironment evaluations. This review emphasizes the necessity for future research efforts to seamlessly incorporate multiple factors and utilize bioinformatics analysis to construct a more comprehensive “interactive map” of the gut microbiota-T cell relationship in CRC. The aim is to establish a solid theoretical basis for the development of highly effective and personalized treatment regimens, ultimately transforming the therapeutic approach to CRC.
AbstractList AbstractThis review delves into the complex and multi-layered mechanisms that govern the interaction between gut microbiota and T cells in the context of colorectal cancer (CRC), revealing a novel “microbiota-immune regulatory landscape” within the tumor microenvironment. As CRC progresses, the gut microbiota experiences a significant transformation in both its composition and metabolic patterns. On one hand, specific microbial entities within the gut microbiota can directly engage with T cells, functioning as “immunological triggers” that shape T-cell behavior. Simultaneously, microbial metabolites, such as short-chain fatty acids and bile acids, serve as “molecular regulators” that intricately govern T-cell function and differentiation, fine-tuning the immune response. On the other hand, the quorum-sensing mechanism, a recently recognized communication network among bacteria, also plays a pivotal role in orchestrating T-cell immunity. Additionally, the gut microbiota forms an intriguing connection with the neuro-immune regulatory axis, a largely unexplored “territory” in CRC research. Regarding treatment strategies, a diverse array of intervention approaches—including dietary modifications, the utilization of probiotics, bacteriophages, and targeted antibiotic therapies—offer promising prospects for restoring the equilibrium of the gut microbiota, thereby acting as “ecosystem renovators” that impede tumor initiation and progression. Nevertheless, the current research landscape in this field is fraught with challenges. These include significant variations in microbial composition, dietary preferences, and tumor microenvironments among individuals, a lack of large-scale cohort studies, and insufficient research that integrates tumor mutation analysis, gut microbiota investigations, and immune microenvironment evaluations. This review emphasizes the necessity for future research efforts to seamlessly incorporate multiple factors and utilize bioinformatics analysis to construct a more comprehensive “interactive map” of the gut microbiota-T cell relationship in CRC. The aim is to establish a solid theoretical basis for the development of highly effective and personalized treatment regimens, ultimately transforming the therapeutic approach to CRC.
This review delves into the complex and multi-layered mechanisms that govern the interaction between gut microbiota and T cells in the context of colorectal cancer (CRC), revealing a novel “microbiota-immune regulatory landscape” within the tumor microenvironment. As CRC progresses, the gut microbiota experiences a significant transformation in both its composition and metabolic patterns. On one hand, specific microbial entities within the gut microbiota can directly engage with T cells, functioning as “immunological triggers” that shape T-cell behavior. Simultaneously, microbial metabolites, such as short-chain fatty acids and bile acids, serve as “molecular regulators” that intricately govern T-cell function and differentiation, fine-tuning the immune response. On the other hand, the quorum-sensing mechanism, a recently recognized communication network among bacteria, also plays a pivotal role in orchestrating T-cell immunity. Additionally, the gut microbiota forms an intriguing connection with the neuro-immune regulatory axis, a largely unexplored “territory” in CRC research. Regarding treatment strategies, a diverse array of intervention approaches—including dietary modifications, the utilization of probiotics, bacteriophages, and targeted antibiotic therapies—offer promising prospects for restoring the equilibrium of the gut microbiota, thereby acting as “ecosystem renovators” that impede tumor initiation and progression. Nevertheless, the current research landscape in this field is fraught with challenges. These include significant variations in microbial composition, dietary preferences, and tumor microenvironments among individuals, a lack of large-scale cohort studies, and insufficient research that integrates tumor mutation analysis, gut microbiota investigations, and immune microenvironment evaluations. This review emphasizes the necessity for future research efforts to seamlessly incorporate multiple factors and utilize bioinformatics analysis to construct a more comprehensive “interactive map” of the gut microbiota-T cell relationship in CRC. The aim is to establish a solid theoretical basis for the development of highly effective and personalized treatment regimens, ultimately transforming the therapeutic approach to CRC.
ArticleNumber 103807
Author Jian, Chu
Xinyue, Wu
Zhanbo, Qu
Jing, Zhuang
Shuwen, Han
Yinhang, Wu
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  givenname: Qu
  surname: Zhanbo
  fullname: Zhanbo, Qu
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  givenname: Han
  surname: Shuwen
  fullname: Shuwen, Han
  email: shuwenhan985@163.com, shuwenhan@zjhu.edu.cn
  organization: Huzhou Central Hospital, Affiliated Central Hospital Huzhou University, No.1558, Sanhuan North Road, Wuxing District, Huzhou, Zhejiang Province 313000, People's Republic of China
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Issue 6
Keywords Gut microbiota
intestinal epithelial cells
effector memory
inflammatory bowel diseases
Clostridiales strains
Colorectal cancer
inhibitors of differentiation 2
tertiary lymphoid structures
Lactobacillus rhamnosus GG
NLR family pyrin domain containing 3
bone marrow-derived dendritic cells
Sini Decoction
azoxymethane
tumor-associated macrophages
Abelmoschus manihot
box transcription factor 13
all-trans-retinoic acid
mesenteric lymph node
Metabolites
ketogenic diet
free fatty acid receptor 2
interleukin
metagenome-wide association study
hepatocellular carcinoma
N-3-oxododecanoyl-L-homoserine lactone
quorum sensing
Toll-like receptor 2
sex-determining region Y
Helicobacter Aciclocus
dextran sulfate sodium
T-helper 1 cells
traditional Chinese medicine
inflammatory bowel disease-associated CRCs
autoinducer-2
germinal center
tissue resident memory T
histone deacetylase
high-fatty-diet
regulatory T cells
Fusobacterium nucleatum
polymorphonuclear-myeloid-derived suppressor cells
T cell immunity
follicular helper T
IPA
Quxie Capsule
short-chain fatty acids
peroxisome proliferator-activated receptor gamma
transforming growth factor-β-activated kinase-1
Indole-3-Propionic Acid
TAM
HFD
IECs
TRM
MLN
atRA
Tfh
FFAR2
Th1
BM-DCs
QS
IL
DSS
QX
EM
HCC
AM
LGG
PPARγ
MGWAS
OdDHL
CRC
IBD-CRCs
PMN-MDSCs
TLR2
HDAC
TCM
SND
IBD
AI-2
TAK1
CC4
NLRP3
KD
SRY
Sox13
GC
TLSs
AOM
Tregs
Fn
Hhep
ID2
SCFAs
Language English
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Snippet This review delves into the complex and multi-layered mechanisms that govern the interaction between gut microbiota and T cells in the context of colorectal...
AbstractThis review delves into the complex and multi-layered mechanisms that govern the interaction between gut microbiota and T cells in the context of...
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SubjectTerms Allergy and Immunology
Animals
Colorectal cancer
Colorectal Neoplasms - immunology
Colorectal Neoplasms - metabolism
Colorectal Neoplasms - microbiology
Colorectal Neoplasms - therapy
Gastrointestinal Microbiome - immunology
Gut microbiota
Humans
Metabolites
T cell immunity
T-Lymphocytes - immunology
T-Lymphocytes - metabolism
Tumor Microenvironment - immunology
Title Interaction between gut microbiota and T cell immunity in colorectal cancer
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https://dx.doi.org/10.1016/j.autrev.2025.103807
https://www.ncbi.nlm.nih.gov/pubmed/40139455
Volume 24
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