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Systemic lupus erythematosus in the light of the regulatory effects of galectin-1 on T-cell function.

Authors :
Hornung Á
Monostori É
Kovács L
Source :
Lupus [Lupus] 2017 Apr; Vol. 26 (4), pp. 339-347. Date of Electronic Publication: 2017 Jan 18.
Publication Year :
2017

Abstract

Galectin-1 is an endogenous immunoregulatory lectin-type protein. Its most important effects are the inhibition of the differentiation and cytokine production of Th1 and Th17 cells, and the induction of apoptosis of activated T-cells. Galectin-1 has been identified as a key molecule in antitumor immune surveillance, and data are accumulating about the pathogenic role of its deficiency, and the beneficial effects of its administration in various autoimmune disease models. Initial animal and human studies strongly suggest deficiencies in both galectin-1 production and responsiveness in systemic lupus erythematosus (SLE) T-cells. Since lupus features widespread abnormalities in T-cell activation, differentiation and viability, in this review the authors wished to highlight potential points in T-cell signalling processes that may be influenced by galectin-1. These points include GM-1 ganglioside-mediated lipid raft aggregation, early activation signalling steps involving p56Lck, the exchange of the CD3 ζ-ZAP-70 to the FcRγ-Syk pathway, defective mitogen-activated protein kinase pathway activation, impaired regulatory T-cell function, the failure to suppress the activity of interleukin 17 (IL-17) producing T-cells, and decreased suppression of the PI3K-mTOR pathway by phosphatase and tensin homolog (PTEN). These findings place galectin-1 into the group of potential pathogenic molecules in SLE.

Details

Language :
English
ISSN :
1477-0962
Volume :
26
Issue :
4
Database :
MEDLINE
Journal :
Lupus
Publication Type :
Academic Journal
Accession number :
28100106
Full Text :
https://doi.org/10.1177/0961203316686846