Galectins in the Pathogenesis of Rheumatoid Arthritis

• Published in: Journal of clinical & cellular immunology Vol. 4; no. 5
• Main Authors: Li, Song, Yu, Yangsheng, Koehn, Christopher D, Zhang, Zhixin, Su, Kaihong
• Format: Journal Article
• Language: English
• Published: United States 30.09.2013
• Subjects: Galectin; Fibroblast-like synoviocytes; Inflammation; T cells; Pathogenesis; Rheumatoid arthritis
• ISSN: 2155-9899; 2155-9899
• DOI: 10.4172/2155-9899.1000164

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.