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-ZAP-70 to the FcR3-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.
| Original language | English |
|---|---|
| Pages (from-to) | 339-347 |
| Number of pages | 9 |
| Journal | Lupus |
| Volume | 26 |
| Issue number | 4 |
| DOIs | |
| Publication status | Published - Apr 1 2017 |
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Keywords
- apoptosis
- Galectin-1
- GM-1 ganglioside
- immunoregulation
- SLE
- T-cell dysfunction
ASJC Scopus subject areas
- Rheumatology
Cite this
Systemic lupus erythematosus in the light of the regulatory effects of galectin-1 on T-cell function. / Hornung, ; Monostori, E.; Kovács, L.
In: Lupus, Vol. 26, No. 4, 01.04.2017, p. 339-347.Research output: Contribution to journal › Review article
}
TY - JOUR
T1 - Systemic lupus erythematosus in the light of the regulatory effects of galectin-1 on T-cell function
AU - Hornung,
AU - Monostori, E.
AU - Kovács, L.
PY - 2017/4/1
Y1 - 2017/4/1
N2 - 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-ZAP-70 to the FcR3-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.
AB - 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-ZAP-70 to the FcR3-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.
KW - apoptosis
KW - Galectin-1
KW - GM-1 ganglioside
KW - immunoregulation
KW - SLE
KW - T-cell dysfunction
UR - http://www.scopus.com/inward/record.url?scp=85015731768&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85015731768&partnerID=8YFLogxK
U2 - 10.1177/0961203316686846
DO - 10.1177/0961203316686846
M3 - Review article
C2 - 28100106
AN - SCOPUS:85015731768
VL - 26
SP - 339
EP - 347
JO - Lupus
JF - Lupus
SN - 0961-2033
IS - 4
ER -