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Ann N Y Acad Sci. 2012 Apr;1253:206-21. doi: 10.1111/j.1749-6632.2012.06479.x.

Beyond glycoproteins as galectin counterreceptors: tumor-effector T cell growth control via ganglioside GM1 [corrected].

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  • 1Department of Neurology and Neurosciences, New Jersey, Medical School-University of Medicine and Dentistry of New Jersey, Newark, USA. ledeenro@umdnj.edu

Erratum in

  • Ann N Y Acad Sci. 2012 Jul;1258:191.

Abstract

Glycoprotein glycan chains, by virtue of structure, topology of presentation and connection to signal-inducing units, are functional galectin counterreceptors. As example, cross-linking of the α(5)β(1) integrin by galectin-1 on carcinoma cells leads to G(1) arrest or anoikis. Contact-dependent switching from proliferation to differentiation in cultured neuroblastoma cells (SK-N-MC) also utilizes galectin-1. Activity enhancement of a cell surface sialidase underlies the shift in glycan display to ganglioside GM1. Its pentasaccharide within microdomains becomes the target. Similarly, this recognition pair is upregulated upon T cell activation. Cross-linking of GM1 along with associated α(4)/α(5)β(1) integrins elicits Ca(2+)-influx via TRPC5 channels as the relevant response for T effector cell (T(eff)) suppression. Unlike T(eff) cells from wild-type mice, those from genetically altered mice lacking GM1 are not suppressed by galectin-1 or regulatory T cells. Similarly, in the context of GM1 deficiency in NOD mice, T(eff) cells are associated with resistance to regulatory T cell suppression, which is reversed by applied GM1. The broad array of glycosphingolipid structures suggests the possible existence of several novel counterreceptors targeted to endogenous lectins, with sulfatide-galectin-4 interplay within apical delivery serving as recent example.

© 2012 New York Academy of Sciences.

PMID:
22524425
[PubMed - indexed for MEDLINE]
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