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Galectins in the Pathogenesis of Rheumatoid Arthritis

Rheumatoid arthritis (RA) is a complex and common systemic autoimmune disease characterized by synovial inflammation and hyperplasia. Multiple proteins, cells, and pathways have been identified to contribute to the pathogenesis of RA. Galectins are a group of lectins that bind to β-galactoside carbo...

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Detalles Bibliográficos
Autores principales: Li, Song, Yu, Yangsheng, Koehn, Christopher D, Zhang, Zhixin, Su, Kaihong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3886720/
https://www.ncbi.nlm.nih.gov/pubmed/24416634
http://dx.doi.org/10.4172/2155-9899.1000164
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author Li, Song
Yu, Yangsheng
Koehn, Christopher D
Zhang, Zhixin
Su, Kaihong
author_facet Li, Song
Yu, Yangsheng
Koehn, Christopher D
Zhang, Zhixin
Su, Kaihong
author_sort Li, Song
collection PubMed
description Rheumatoid arthritis (RA) is a complex and common systemic autoimmune disease characterized by synovial inflammation and hyperplasia. Multiple proteins, cells, and pathways have been identified to contribute to the pathogenesis of RA. Galectins are a group of lectins that bind to β-galactoside carbohydrates on the cell surface and in the extracellular matrix. They are expressed in a wide variety of tissues and organs with the highest expression in the immune system. Galectins are potent immune regulators and modulate a range of pathological processes, such as inflammation, autoimmunity, and cancer. Accumulated evidence shows that several family members of galectins play positive or negative roles in the disease development of RA, through their effects on T and B lymphocytes, myeloid lineage cells, and fibroblast-like synoviocytes. In this review, we will summarize the function of different galectins in immune modulation and their distinct roles in RA pathogenesis.
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spelling pubmed-38867202014-01-09 Galectins in the Pathogenesis of Rheumatoid Arthritis Li, Song Yu, Yangsheng Koehn, Christopher D Zhang, Zhixin Su, Kaihong J Clin Cell Immunol Article Rheumatoid arthritis (RA) is a complex and common systemic autoimmune disease characterized by synovial inflammation and hyperplasia. Multiple proteins, cells, and pathways have been identified to contribute to the pathogenesis of RA. Galectins are a group of lectins that bind to β-galactoside carbohydrates on the cell surface and in the extracellular matrix. They are expressed in a wide variety of tissues and organs with the highest expression in the immune system. Galectins are potent immune regulators and modulate a range of pathological processes, such as inflammation, autoimmunity, and cancer. Accumulated evidence shows that several family members of galectins play positive or negative roles in the disease development of RA, through their effects on T and B lymphocytes, myeloid lineage cells, and fibroblast-like synoviocytes. In this review, we will summarize the function of different galectins in immune modulation and their distinct roles in RA pathogenesis. 2013-09-30 /pmc/articles/PMC3886720/ /pubmed/24416634 http://dx.doi.org/10.4172/2155-9899.1000164 Text en Copyright: © 2013 Li S, et al. http://creativecommons.org/licenses/by/2.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Article
Li, Song
Yu, Yangsheng
Koehn, Christopher D
Zhang, Zhixin
Su, Kaihong
Galectins in the Pathogenesis of Rheumatoid Arthritis
title Galectins in the Pathogenesis of Rheumatoid Arthritis
title_full Galectins in the Pathogenesis of Rheumatoid Arthritis
title_fullStr Galectins in the Pathogenesis of Rheumatoid Arthritis
title_full_unstemmed Galectins in the Pathogenesis of Rheumatoid Arthritis
title_short Galectins in the Pathogenesis of Rheumatoid Arthritis
title_sort galectins in the pathogenesis of rheumatoid arthritis
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3886720/
https://www.ncbi.nlm.nih.gov/pubmed/24416634
http://dx.doi.org/10.4172/2155-9899.1000164
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