Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Ledeen, R.W. et al.

Robert W. Ledeen, Gusheng Wu, Sabine André, David Bleich, Guillemette Huet, Herbert Kaltner, Jürgen Kopitz, Hans-Joachim Gabius, Gusheng Wu, Sabine André, David Bleich, Guillemette Huet, Herbert Kaltner, Jürgen Kopitz, Hans-Joachim Gabius,

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

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.[1]

References

Beyond glycoproteins as galectin counterreceptors: tumor-effector T cell growth control via ganglioside GM1 [corrected]. Ledeen, R.W., Wu, G., André, S., Bleich, D., Huet, G., Kaltner, H., Kopitz, J., Gabius, H.J. Ann. N. Y. Acad. Sci. (2012) [Pubmed]

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