Untangling Galectin-Driven Regulatory Circuits in Autoimmune Inflammation

Although progress has been made in understanding the mechanisms implicated in the pathogenesis of autoimmune inflammation, studies aimed at identifying the mediators of these pathways will be necessary to develop more selective therapies. Galectins, a family of glycan-binding proteins, play central...

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Publicado: 2018
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Acceso en línea:https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_14714914_v24_n4_p348_Toscano
http://hdl.handle.net/20.500.12110/paper_14714914_v24_n4_p348_Toscano
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spelling paper:paper_14714914_v24_n4_p348_Toscano2023-06-08T16:17:21Z Untangling Galectin-Driven Regulatory Circuits in Autoimmune Inflammation autoimmunity chronic inflammation galectins glycans immunoregulation ecalectin galectin galectin 2 galectin 3 gamma interferon glycan interleukin 10 interleukin 17 interleukin 1beta interleukin 27 tumor necrosis factor biological factor galectin apoptosis astrocyte autoimmune disease CD4+ T lymphocyte CD8+ T lymphocyte collagen-induced arthritis Crohn disease dendritic cell endothelium cell experimental autoimmune encephalomyelitis glycosylation human immunocompetent cell immunological tolerance immunomodulation inflammation inflammatory bowel disease insulin dependent diabetes mellitus intestine flora lymphocytic infiltration macrophage microglia multiple sclerosis nervous system inflammation nonhuman protein carbohydrate interaction protein expression protein function regulatory T lymphocyte Review rheumatoid arthritis systemic lupus erythematosus Th1 cell Th17 cell ulcerative colitis upregulation adverse drug reaction animal autoimmune disease autoimmunity drug effect inflammation metabolism Animals Autoimmune Diseases Autoimmunity Biological Factors Drug-Related Side Effects and Adverse Reactions Galectins Humans Inflammation Although progress has been made in understanding the mechanisms implicated in the pathogenesis of autoimmune inflammation, studies aimed at identifying the mediators of these pathways will be necessary to develop more selective therapies. Galectins, a family of glycan-binding proteins, play central roles in immune cell homeostasis. Whereas some members of this family trigger regulatory programs that promote resolution of inflammation, others contribute to perpetuate autoimmune processes. We discuss the roles of endogenous galectins and their specific glycosylated ligands in shaping autoimmune responses by fueling, extinguishing, or rewiring immune circuits. Understanding the relevance of galectin–glycan interactions in autoimmune inflammation could help to uncover novel pathways of tolerance breakdown, define molecular signatures for patient stratification and therapy responses, and open new avenues for immune intervention. © 2018 Elsevier Ltd 2018 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_14714914_v24_n4_p348_Toscano http://hdl.handle.net/20.500.12110/paper_14714914_v24_n4_p348_Toscano
institution Universidad de Buenos Aires
institution_str I-28
repository_str R-134
collection Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic autoimmunity
chronic inflammation
galectins
glycans
immunoregulation
ecalectin
galectin
galectin 2
galectin 3
gamma interferon
glycan
interleukin 10
interleukin 17
interleukin 1beta
interleukin 27
tumor necrosis factor
biological factor
galectin
apoptosis
astrocyte
autoimmune disease
CD4+ T lymphocyte
CD8+ T lymphocyte
collagen-induced arthritis
Crohn disease
dendritic cell
endothelium cell
experimental autoimmune encephalomyelitis
glycosylation
human
immunocompetent cell
immunological tolerance
immunomodulation
inflammation
inflammatory bowel disease
insulin dependent diabetes mellitus
intestine flora
lymphocytic infiltration
macrophage
microglia
multiple sclerosis
nervous system inflammation
nonhuman
protein carbohydrate interaction
protein expression
protein function
regulatory T lymphocyte
Review
rheumatoid arthritis
systemic lupus erythematosus
Th1 cell
Th17 cell
ulcerative colitis
upregulation
adverse drug reaction
animal
autoimmune disease
autoimmunity
drug effect
inflammation
metabolism
Animals
Autoimmune Diseases
Autoimmunity
Biological Factors
Drug-Related Side Effects and Adverse Reactions
Galectins
Humans
Inflammation
spellingShingle autoimmunity
chronic inflammation
galectins
glycans
immunoregulation
ecalectin
galectin
galectin 2
galectin 3
gamma interferon
glycan
interleukin 10
interleukin 17
interleukin 1beta
interleukin 27
tumor necrosis factor
biological factor
galectin
apoptosis
astrocyte
autoimmune disease
CD4+ T lymphocyte
CD8+ T lymphocyte
collagen-induced arthritis
Crohn disease
dendritic cell
endothelium cell
experimental autoimmune encephalomyelitis
glycosylation
human
immunocompetent cell
immunological tolerance
immunomodulation
inflammation
inflammatory bowel disease
insulin dependent diabetes mellitus
intestine flora
lymphocytic infiltration
macrophage
microglia
multiple sclerosis
nervous system inflammation
nonhuman
protein carbohydrate interaction
protein expression
protein function
regulatory T lymphocyte
Review
rheumatoid arthritis
systemic lupus erythematosus
Th1 cell
Th17 cell
ulcerative colitis
upregulation
adverse drug reaction
animal
autoimmune disease
autoimmunity
drug effect
inflammation
metabolism
Animals
Autoimmune Diseases
Autoimmunity
Biological Factors
Drug-Related Side Effects and Adverse Reactions
Galectins
Humans
Inflammation
Untangling Galectin-Driven Regulatory Circuits in Autoimmune Inflammation
topic_facet autoimmunity
chronic inflammation
galectins
glycans
immunoregulation
ecalectin
galectin
galectin 2
galectin 3
gamma interferon
glycan
interleukin 10
interleukin 17
interleukin 1beta
interleukin 27
tumor necrosis factor
biological factor
galectin
apoptosis
astrocyte
autoimmune disease
CD4+ T lymphocyte
CD8+ T lymphocyte
collagen-induced arthritis
Crohn disease
dendritic cell
endothelium cell
experimental autoimmune encephalomyelitis
glycosylation
human
immunocompetent cell
immunological tolerance
immunomodulation
inflammation
inflammatory bowel disease
insulin dependent diabetes mellitus
intestine flora
lymphocytic infiltration
macrophage
microglia
multiple sclerosis
nervous system inflammation
nonhuman
protein carbohydrate interaction
protein expression
protein function
regulatory T lymphocyte
Review
rheumatoid arthritis
systemic lupus erythematosus
Th1 cell
Th17 cell
ulcerative colitis
upregulation
adverse drug reaction
animal
autoimmune disease
autoimmunity
drug effect
inflammation
metabolism
Animals
Autoimmune Diseases
Autoimmunity
Biological Factors
Drug-Related Side Effects and Adverse Reactions
Galectins
Humans
Inflammation
description Although progress has been made in understanding the mechanisms implicated in the pathogenesis of autoimmune inflammation, studies aimed at identifying the mediators of these pathways will be necessary to develop more selective therapies. Galectins, a family of glycan-binding proteins, play central roles in immune cell homeostasis. Whereas some members of this family trigger regulatory programs that promote resolution of inflammation, others contribute to perpetuate autoimmune processes. We discuss the roles of endogenous galectins and their specific glycosylated ligands in shaping autoimmune responses by fueling, extinguishing, or rewiring immune circuits. Understanding the relevance of galectin–glycan interactions in autoimmune inflammation could help to uncover novel pathways of tolerance breakdown, define molecular signatures for patient stratification and therapy responses, and open new avenues for immune intervention. © 2018 Elsevier Ltd
title Untangling Galectin-Driven Regulatory Circuits in Autoimmune Inflammation
title_short Untangling Galectin-Driven Regulatory Circuits in Autoimmune Inflammation
title_full Untangling Galectin-Driven Regulatory Circuits in Autoimmune Inflammation
title_fullStr Untangling Galectin-Driven Regulatory Circuits in Autoimmune Inflammation
title_full_unstemmed Untangling Galectin-Driven Regulatory Circuits in Autoimmune Inflammation
title_sort untangling galectin-driven regulatory circuits in autoimmune inflammation
publishDate 2018
url https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_14714914_v24_n4_p348_Toscano
http://hdl.handle.net/20.500.12110/paper_14714914_v24_n4_p348_Toscano
_version_ 1768542472158314496