Tolerogenic dendritic cells in the control of autoimmune neuroinflammation: An emerging role of protein-glycan interactions
During the past decade, a great deal of information has contributed to our understanding of the immunosuppressive pathways that operate during the resolution of autoimmune pathology, including central nervous system (CNS) inflammation. Activation of these pathways is accomplished through the integra...
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paper:paper_10217401_v17_n3_p157_Ilarregui2023-06-08T16:00:01Z Tolerogenic dendritic cells in the control of autoimmune neuroinflammation: An emerging role of protein-glycan interactions Ilarregui, Juan Martín Dendritic cells Experimental autoimmune encephalomyelitis Galectin-1 Interleukin-10 Interleukin-27 Multiple sclerosis Neuroinflammation CD45RB antigen colecalciferol galectin 1 gamma interferon glycan interleukin 10 interleukin 12 interleukin 23 interleukin 27 protein protein kinase Syk STAT3 protein toll like receptor agonist tumor necrosis factor alpha antibody autoimmune disease cell differentiation cell migration central nervous system chronic inflammation conference paper cytokine production cytokine release dendritic cell disease course effector cell encephalomyelitis genotype phenotype correlation helper cell human immune response immunological tolerance immunoregulation multiple sclerosis nerve cell plasticity neuroprotection nonhuman priority journal protein binding protein carbohydrate interaction protein phosphorylation signal transduction T lymphocyte Th1 cell Th17 cell Th2 cell tumor growth Animals Autoimmune Diseases of the Nervous System Dendritic Cells Encephalitis Galectin 1 Humans Immune Tolerance Myelitis Polysaccharides T-Lymphocytes During the past decade, a great deal of information has contributed to our understanding of the immunosuppressive pathways that operate during the resolution of autoimmune pathology, including central nervous system (CNS) inflammation. Activation of these pathways is accomplished through the integration of an intricate network of inhibitory signals and immune suppressive cells, including regulatory T cells, myeloid-derived suppressor cells, 'alternatively activated' macrophages and tolerogenic dendritic cells (DCs). During the course of inflammatory diseases, immature or mature DCs may be licensed by different stimuli (e.g. cytokines, neuropeptides and growth factors) to become tolerogenic and suppress pathogenic T cell responses, thus emphasizing the outstanding plasticity of these cells. Recent findings have shed light to an immunoregulatory circuit by which galectin-1, an endogenous glycan-binding protein, favors the differentiation of regulatory DCs which promote T cell tolerance and contribute to resolution of autoimmune pathology through mechanisms involving IL-27 and IL-10. Together with the ability of galectin-1-glycan interactions to selectively blunt T helper (Th)1 and Th17 responses, this effect provides a rational explanation for the broad immunosuppressive effects of this glycan-binding protein in several experimental models of chronic inflammation and cancer. In this mini review, we will summarize the regulatory signals leading to the differentiation of tolerogenic DCs and their participation in CNS inflammation. In addition, we will underscore recent findings on the emerging role of galectin-glycan interactions in the establishment of immunosuppressive networks during the resolution of chronic inflammation. © 2010 S. Karger AG, Basel. Fil:Ilarregui, J.M. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. 2010 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_10217401_v17_n3_p157_Ilarregui http://hdl.handle.net/20.500.12110/paper_10217401_v17_n3_p157_Ilarregui |
| institution |
Universidad de Buenos Aires |
| institution_str |
I-28 |
| repository_str |
R-134 |
| collection |
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) |
| topic |
Dendritic cells Experimental autoimmune encephalomyelitis Galectin-1 Interleukin-10 Interleukin-27 Multiple sclerosis Neuroinflammation CD45RB antigen colecalciferol galectin 1 gamma interferon glycan interleukin 10 interleukin 12 interleukin 23 interleukin 27 protein protein kinase Syk STAT3 protein toll like receptor agonist tumor necrosis factor alpha antibody autoimmune disease cell differentiation cell migration central nervous system chronic inflammation conference paper cytokine production cytokine release dendritic cell disease course effector cell encephalomyelitis genotype phenotype correlation helper cell human immune response immunological tolerance immunoregulation multiple sclerosis nerve cell plasticity neuroprotection nonhuman priority journal protein binding protein carbohydrate interaction protein phosphorylation signal transduction T lymphocyte Th1 cell Th17 cell Th2 cell tumor growth Animals Autoimmune Diseases of the Nervous System Dendritic Cells Encephalitis Galectin 1 Humans Immune Tolerance Myelitis Polysaccharides T-Lymphocytes |
| spellingShingle |
Dendritic cells Experimental autoimmune encephalomyelitis Galectin-1 Interleukin-10 Interleukin-27 Multiple sclerosis Neuroinflammation CD45RB antigen colecalciferol galectin 1 gamma interferon glycan interleukin 10 interleukin 12 interleukin 23 interleukin 27 protein protein kinase Syk STAT3 protein toll like receptor agonist tumor necrosis factor alpha antibody autoimmune disease cell differentiation cell migration central nervous system chronic inflammation conference paper cytokine production cytokine release dendritic cell disease course effector cell encephalomyelitis genotype phenotype correlation helper cell human immune response immunological tolerance immunoregulation multiple sclerosis nerve cell plasticity neuroprotection nonhuman priority journal protein binding protein carbohydrate interaction protein phosphorylation signal transduction T lymphocyte Th1 cell Th17 cell Th2 cell tumor growth Animals Autoimmune Diseases of the Nervous System Dendritic Cells Encephalitis Galectin 1 Humans Immune Tolerance Myelitis Polysaccharides T-Lymphocytes Ilarregui, Juan Martín Tolerogenic dendritic cells in the control of autoimmune neuroinflammation: An emerging role of protein-glycan interactions |
| topic_facet |
Dendritic cells Experimental autoimmune encephalomyelitis Galectin-1 Interleukin-10 Interleukin-27 Multiple sclerosis Neuroinflammation CD45RB antigen colecalciferol galectin 1 gamma interferon glycan interleukin 10 interleukin 12 interleukin 23 interleukin 27 protein protein kinase Syk STAT3 protein toll like receptor agonist tumor necrosis factor alpha antibody autoimmune disease cell differentiation cell migration central nervous system chronic inflammation conference paper cytokine production cytokine release dendritic cell disease course effector cell encephalomyelitis genotype phenotype correlation helper cell human immune response immunological tolerance immunoregulation multiple sclerosis nerve cell plasticity neuroprotection nonhuman priority journal protein binding protein carbohydrate interaction protein phosphorylation signal transduction T lymphocyte Th1 cell Th17 cell Th2 cell tumor growth Animals Autoimmune Diseases of the Nervous System Dendritic Cells Encephalitis Galectin 1 Humans Immune Tolerance Myelitis Polysaccharides T-Lymphocytes |
| description |
During the past decade, a great deal of information has contributed to our understanding of the immunosuppressive pathways that operate during the resolution of autoimmune pathology, including central nervous system (CNS) inflammation. Activation of these pathways is accomplished through the integration of an intricate network of inhibitory signals and immune suppressive cells, including regulatory T cells, myeloid-derived suppressor cells, 'alternatively activated' macrophages and tolerogenic dendritic cells (DCs). During the course of inflammatory diseases, immature or mature DCs may be licensed by different stimuli (e.g. cytokines, neuropeptides and growth factors) to become tolerogenic and suppress pathogenic T cell responses, thus emphasizing the outstanding plasticity of these cells. Recent findings have shed light to an immunoregulatory circuit by which galectin-1, an endogenous glycan-binding protein, favors the differentiation of regulatory DCs which promote T cell tolerance and contribute to resolution of autoimmune pathology through mechanisms involving IL-27 and IL-10. Together with the ability of galectin-1-glycan interactions to selectively blunt T helper (Th)1 and Th17 responses, this effect provides a rational explanation for the broad immunosuppressive effects of this glycan-binding protein in several experimental models of chronic inflammation and cancer. In this mini review, we will summarize the regulatory signals leading to the differentiation of tolerogenic DCs and their participation in CNS inflammation. In addition, we will underscore recent findings on the emerging role of galectin-glycan interactions in the establishment of immunosuppressive networks during the resolution of chronic inflammation. © 2010 S. Karger AG, Basel. |
| author |
Ilarregui, Juan Martín |
| author_facet |
Ilarregui, Juan Martín |
| author_sort |
Ilarregui, Juan Martín |
| title |
Tolerogenic dendritic cells in the control of autoimmune neuroinflammation: An emerging role of protein-glycan interactions |
| title_short |
Tolerogenic dendritic cells in the control of autoimmune neuroinflammation: An emerging role of protein-glycan interactions |
| title_full |
Tolerogenic dendritic cells in the control of autoimmune neuroinflammation: An emerging role of protein-glycan interactions |
| title_fullStr |
Tolerogenic dendritic cells in the control of autoimmune neuroinflammation: An emerging role of protein-glycan interactions |
| title_full_unstemmed |
Tolerogenic dendritic cells in the control of autoimmune neuroinflammation: An emerging role of protein-glycan interactions |
| title_sort |
tolerogenic dendritic cells in the control of autoimmune neuroinflammation: an emerging role of protein-glycan interactions |
| publishDate |
2010 |
| url |
https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_10217401_v17_n3_p157_Ilarregui http://hdl.handle.net/20.500.12110/paper_10217401_v17_n3_p157_Ilarregui |
| work_keys_str_mv |
AT ilarreguijuanmartin tolerogenicdendriticcellsinthecontrolofautoimmuneneuroinflammationanemergingroleofproteinglycaninteractions |
| _version_ |
1768542997684682752 |