Integration of lectin-glycan recognition systems and immune cell networks in CNS inflammation
Multiple sclerosis (MS) is a progressive degenerative disorder of the central nervous system (CNS), characterized by inflammation, demyelination and axonal loss. While the majority of MS patients experience relapsing-remitting symptoms followed by a secondary progressive phase, about 10-15% patients...
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todo:paper_13596101_v25_n3_p247_MendezHuergo2023-10-03T16:10:38Z Integration of lectin-glycan recognition systems and immune cell networks in CNS inflammation Mendez-Huergo, S.P. Maller, S.M. Farez, M.F. Mariño, K. Correale, J. Rabinovich, G.A. C-type lectins Galectins Glycans Multiple sclerosis Siglecs cytotoxic T lymphocyte antigen 4 galectin interleukin 10 interleukin 13 interleukin 17 interleukin 17F interleukin 27 interleukin 4 interleukin 5 lectin major histocompatibility antigen sialic acid binding immunoglobulin like lectin sialoadhesin cytokine galectin lectin polysaccharide allergic encephalomyelitis astrocyte CD4+ T lymphocyte CD8+ T lymphocyte cell death cell population cytokine production cytokine release dendritic cell disease severity experimental autoimmune encephalomyelitis glycobiology glycosylation human immune response immunocompetent cell immunopathogenesis immunoregulation macrophage multiple sclerosis nonhuman oligodendroglia phenotype priority journal protein expression protein function protein protein interaction short survey T lymphocyte upregulation animal central nervous system immunology multiple sclerosis pathology Animals Central Nervous System Cytokines Dendritic Cells Galectins Humans Lectins, C-Type Multiple Sclerosis Polysaccharides T-Lymphocytes Multiple sclerosis (MS) is a progressive degenerative disorder of the central nervous system (CNS), characterized by inflammation, demyelination and axonal loss. While the majority of MS patients experience relapsing-remitting symptoms followed by a secondary progressive phase, about 10-15% patients exhibit a primary progressive disease involving continuous progression from its onset. Here we review the role of lectin-glycan recognition systems, including those concerning siglecs, C-type lectins and galectins in the pathogenesis of MS and experimental autoimmune encephalomyelitis. Particularly, we will focus on the role of galectins in the fate of T cells, dendritic cells and CNS cell populations. Understanding the regulatory circuits governed by lectin-glycan interactions and their association with disease-associated cytokine networks will contribute to develop novel therapeutic strategies in MS. © 2014 Elsevier Ltd. JOUR info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/2.5/ar http://hdl.handle.net/20.500.12110/paper_13596101_v25_n3_p247_MendezHuergo |
| institution |
Universidad de Buenos Aires |
| institution_str |
I-28 |
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R-134 |
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Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) |
| topic |
C-type lectins Galectins Glycans Multiple sclerosis Siglecs cytotoxic T lymphocyte antigen 4 galectin interleukin 10 interleukin 13 interleukin 17 interleukin 17F interleukin 27 interleukin 4 interleukin 5 lectin major histocompatibility antigen sialic acid binding immunoglobulin like lectin sialoadhesin cytokine galectin lectin polysaccharide allergic encephalomyelitis astrocyte CD4+ T lymphocyte CD8+ T lymphocyte cell death cell population cytokine production cytokine release dendritic cell disease severity experimental autoimmune encephalomyelitis glycobiology glycosylation human immune response immunocompetent cell immunopathogenesis immunoregulation macrophage multiple sclerosis nonhuman oligodendroglia phenotype priority journal protein expression protein function protein protein interaction short survey T lymphocyte upregulation animal central nervous system immunology multiple sclerosis pathology Animals Central Nervous System Cytokines Dendritic Cells Galectins Humans Lectins, C-Type Multiple Sclerosis Polysaccharides T-Lymphocytes |
| spellingShingle |
C-type lectins Galectins Glycans Multiple sclerosis Siglecs cytotoxic T lymphocyte antigen 4 galectin interleukin 10 interleukin 13 interleukin 17 interleukin 17F interleukin 27 interleukin 4 interleukin 5 lectin major histocompatibility antigen sialic acid binding immunoglobulin like lectin sialoadhesin cytokine galectin lectin polysaccharide allergic encephalomyelitis astrocyte CD4+ T lymphocyte CD8+ T lymphocyte cell death cell population cytokine production cytokine release dendritic cell disease severity experimental autoimmune encephalomyelitis glycobiology glycosylation human immune response immunocompetent cell immunopathogenesis immunoregulation macrophage multiple sclerosis nonhuman oligodendroglia phenotype priority journal protein expression protein function protein protein interaction short survey T lymphocyte upregulation animal central nervous system immunology multiple sclerosis pathology Animals Central Nervous System Cytokines Dendritic Cells Galectins Humans Lectins, C-Type Multiple Sclerosis Polysaccharides T-Lymphocytes Mendez-Huergo, S.P. Maller, S.M. Farez, M.F. Mariño, K. Correale, J. Rabinovich, G.A. Integration of lectin-glycan recognition systems and immune cell networks in CNS inflammation |
| topic_facet |
C-type lectins Galectins Glycans Multiple sclerosis Siglecs cytotoxic T lymphocyte antigen 4 galectin interleukin 10 interleukin 13 interleukin 17 interleukin 17F interleukin 27 interleukin 4 interleukin 5 lectin major histocompatibility antigen sialic acid binding immunoglobulin like lectin sialoadhesin cytokine galectin lectin polysaccharide allergic encephalomyelitis astrocyte CD4+ T lymphocyte CD8+ T lymphocyte cell death cell population cytokine production cytokine release dendritic cell disease severity experimental autoimmune encephalomyelitis glycobiology glycosylation human immune response immunocompetent cell immunopathogenesis immunoregulation macrophage multiple sclerosis nonhuman oligodendroglia phenotype priority journal protein expression protein function protein protein interaction short survey T lymphocyte upregulation animal central nervous system immunology multiple sclerosis pathology Animals Central Nervous System Cytokines Dendritic Cells Galectins Humans Lectins, C-Type Multiple Sclerosis Polysaccharides T-Lymphocytes |
| description |
Multiple sclerosis (MS) is a progressive degenerative disorder of the central nervous system (CNS), characterized by inflammation, demyelination and axonal loss. While the majority of MS patients experience relapsing-remitting symptoms followed by a secondary progressive phase, about 10-15% patients exhibit a primary progressive disease involving continuous progression from its onset. Here we review the role of lectin-glycan recognition systems, including those concerning siglecs, C-type lectins and galectins in the pathogenesis of MS and experimental autoimmune encephalomyelitis. Particularly, we will focus on the role of galectins in the fate of T cells, dendritic cells and CNS cell populations. Understanding the regulatory circuits governed by lectin-glycan interactions and their association with disease-associated cytokine networks will contribute to develop novel therapeutic strategies in MS. © 2014 Elsevier Ltd. |
| format |
JOUR |
| author |
Mendez-Huergo, S.P. Maller, S.M. Farez, M.F. Mariño, K. Correale, J. Rabinovich, G.A. |
| author_facet |
Mendez-Huergo, S.P. Maller, S.M. Farez, M.F. Mariño, K. Correale, J. Rabinovich, G.A. |
| author_sort |
Mendez-Huergo, S.P. |
| title |
Integration of lectin-glycan recognition systems and immune cell networks in CNS inflammation |
| title_short |
Integration of lectin-glycan recognition systems and immune cell networks in CNS inflammation |
| title_full |
Integration of lectin-glycan recognition systems and immune cell networks in CNS inflammation |
| title_fullStr |
Integration of lectin-glycan recognition systems and immune cell networks in CNS inflammation |
| title_full_unstemmed |
Integration of lectin-glycan recognition systems and immune cell networks in CNS inflammation |
| title_sort |
integration of lectin-glycan recognition systems and immune cell networks in cns inflammation |
| url |
http://hdl.handle.net/20.500.12110/paper_13596101_v25_n3_p247_MendezHuergo |
| work_keys_str_mv |
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| _version_ |
1782024753389764608 |