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TNFSF14 (LIGHT) in intestinal inflammation: balancing immune activation and resolution in IBD
by
Jones, Joanne L.
, Mousa, Hani S.
, Mousa, Rabia S.
, Invernizzi, Pietro
in
Animals
/ BTLA (B and T lymphocyte attenuator)
/ Chemokines
/ Clinical trials
/ Crohn's disease
/ Cytokines
/ DcR3 (TNFRSF6B)
/ Gastrointestinal tract
/ Genes
/ Glycoproteins
/ Growth factors
/ Herpes viruses
/ Homeostasis
/ Humans
/ HVEM (TNFRSF14)
/ Immune response
/ Immunology
/ Immunoregulation
/ Inflammation
/ Inflammation - immunology
/ Inflammatory bowel disease
/ inflammatory bowel disease (IBD)
/ Inflammatory bowel diseases
/ Inflammatory Bowel Diseases - immunology
/ Inflammatory Bowel Diseases - metabolism
/ Intestinal Mucosa - immunology
/ Intestinal Mucosa - metabolism
/ Intestine
/ Kinases
/ Ligands
/ Light
/ LIGHT (TNFSF14)
/ LTβR (Lymphotoxin-β receptor)
/ Lymphocytes
/ Lymphoma
/ Lymphotoxin
/ Lymphotoxin beta Receptor - immunology
/ Lymphotoxin beta Receptor - metabolism
/ Microbiota
/ Molecular modelling
/ Neutrophils
/ Pathogenesis
/ Proteins
/ Receptors, Tumor Necrosis Factor, Member 14 - immunology
/ Receptors, Tumor Necrosis Factor, Member 14 - metabolism
/ Signal Transduction
/ TNF inhibitors
/ Tumor Necrosis Factor Ligand Superfamily Member 14 - immunology
/ Tumor Necrosis Factor Ligand Superfamily Member 14 - metabolism
/ Tumor necrosis factor-TNF
/ Ulcerative colitis
2025
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TNFSF14 (LIGHT) in intestinal inflammation: balancing immune activation and resolution in IBD
by
Jones, Joanne L.
, Mousa, Hani S.
, Mousa, Rabia S.
, Invernizzi, Pietro
in
Animals
/ BTLA (B and T lymphocyte attenuator)
/ Chemokines
/ Clinical trials
/ Crohn's disease
/ Cytokines
/ DcR3 (TNFRSF6B)
/ Gastrointestinal tract
/ Genes
/ Glycoproteins
/ Growth factors
/ Herpes viruses
/ Homeostasis
/ Humans
/ HVEM (TNFRSF14)
/ Immune response
/ Immunology
/ Immunoregulation
/ Inflammation
/ Inflammation - immunology
/ Inflammatory bowel disease
/ inflammatory bowel disease (IBD)
/ Inflammatory bowel diseases
/ Inflammatory Bowel Diseases - immunology
/ Inflammatory Bowel Diseases - metabolism
/ Intestinal Mucosa - immunology
/ Intestinal Mucosa - metabolism
/ Intestine
/ Kinases
/ Ligands
/ Light
/ LIGHT (TNFSF14)
/ LTβR (Lymphotoxin-β receptor)
/ Lymphocytes
/ Lymphoma
/ Lymphotoxin
/ Lymphotoxin beta Receptor - immunology
/ Lymphotoxin beta Receptor - metabolism
/ Microbiota
/ Molecular modelling
/ Neutrophils
/ Pathogenesis
/ Proteins
/ Receptors, Tumor Necrosis Factor, Member 14 - immunology
/ Receptors, Tumor Necrosis Factor, Member 14 - metabolism
/ Signal Transduction
/ TNF inhibitors
/ Tumor Necrosis Factor Ligand Superfamily Member 14 - immunology
/ Tumor Necrosis Factor Ligand Superfamily Member 14 - metabolism
/ Tumor necrosis factor-TNF
/ Ulcerative colitis
2025
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TNFSF14 (LIGHT) in intestinal inflammation: balancing immune activation and resolution in IBD
by
Jones, Joanne L.
, Mousa, Hani S.
, Mousa, Rabia S.
, Invernizzi, Pietro
in
Animals
/ BTLA (B and T lymphocyte attenuator)
/ Chemokines
/ Clinical trials
/ Crohn's disease
/ Cytokines
/ DcR3 (TNFRSF6B)
/ Gastrointestinal tract
/ Genes
/ Glycoproteins
/ Growth factors
/ Herpes viruses
/ Homeostasis
/ Humans
/ HVEM (TNFRSF14)
/ Immune response
/ Immunology
/ Immunoregulation
/ Inflammation
/ Inflammation - immunology
/ Inflammatory bowel disease
/ inflammatory bowel disease (IBD)
/ Inflammatory bowel diseases
/ Inflammatory Bowel Diseases - immunology
/ Inflammatory Bowel Diseases - metabolism
/ Intestinal Mucosa - immunology
/ Intestinal Mucosa - metabolism
/ Intestine
/ Kinases
/ Ligands
/ Light
/ LIGHT (TNFSF14)
/ LTβR (Lymphotoxin-β receptor)
/ Lymphocytes
/ Lymphoma
/ Lymphotoxin
/ Lymphotoxin beta Receptor - immunology
/ Lymphotoxin beta Receptor - metabolism
/ Microbiota
/ Molecular modelling
/ Neutrophils
/ Pathogenesis
/ Proteins
/ Receptors, Tumor Necrosis Factor, Member 14 - immunology
/ Receptors, Tumor Necrosis Factor, Member 14 - metabolism
/ Signal Transduction
/ TNF inhibitors
/ Tumor Necrosis Factor Ligand Superfamily Member 14 - immunology
/ Tumor Necrosis Factor Ligand Superfamily Member 14 - metabolism
/ Tumor necrosis factor-TNF
/ Ulcerative colitis
2025
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TNFSF14 (LIGHT) in intestinal inflammation: balancing immune activation and resolution in IBD
Journal Article
TNFSF14 (LIGHT) in intestinal inflammation: balancing immune activation and resolution in IBD
2025
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Overview
Inflammatory Bowel Disease (IBD), encompassing Crohn’s disease and ulcerative colitis, is an umbrella term used to describe a group of autoimmune conditions characterized by chronic, relapsing inflammation of the gastrointestinal tract. The tumour necrosis factor superfamily member 14 (TNFSF14), also known as LIGHT, is a pleiotropic cytokine with diverse roles in immune regulation. Here, we review the multifaceted involvement of LIGHT in intestinal inflammation, particularly its dual capacity to both promote immune activation and facilitate inflammation resolution in the context of IBD. We explore the molecular mechanisms of LIGHT signalling through its receptors, Herpes Virus Entry Mediator (HVEM) and Lymphotoxin-β Receptor (LTβR), and how these distinct interactions dictate its pro-inflammatory or regulatory functions. Finally, we review the therapeutic potential of targeting this pathway, highlighting the results of recent clinical trials and exploring future strategies aimed at restoring immune homeostasis in patients with IBD.
Publisher
Frontiers Media SA,Frontiers Media S.A
Subject
/ BTLA (B and T lymphocyte attenuator)
/ Genes
/ Humans
/ inflammatory bowel disease (IBD)
/ Inflammatory Bowel Diseases - immunology
/ Inflammatory Bowel Diseases - metabolism
/ Intestinal Mucosa - immunology
/ Intestinal Mucosa - metabolism
/ Kinases
/ Ligands
/ Light
/ LTβR (Lymphotoxin-β receptor)
/ Lymphoma
/ Lymphotoxin beta Receptor - immunology
/ Lymphotoxin beta Receptor - metabolism
/ Proteins
/ Receptors, Tumor Necrosis Factor, Member 14 - immunology
/ Receptors, Tumor Necrosis Factor, Member 14 - metabolism
/ Tumor Necrosis Factor Ligand Superfamily Member 14 - immunology
/ Tumor Necrosis Factor Ligand Superfamily Member 14 - metabolism
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