Differential glycosylation of TH1, TH2 and TH-17 effector cells selectively regulates susceptibility to cell death

By M. Toscano, Germán A. Bianco, J. Ilarregui, D. Croci, J. Correale, Joseph D. Hernandez, N. Zwirner, F. Poirier, Eleanor M. Riley, L. Baum and 1 more. Nature Immunology, 2007

672 citations recorded by the source corpus.

Subfields: Immunology

View Paper: https://www.semanticscholar.org/paper/cc9cf66b76142b69651d319cc7ff1908228f8142

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In Immunology

1. M. Toscano
2. J. Bluestone
3. Q. Tang
4. Gabriel A. Rabinovich
5. Y. Kooyk
6. Shimon Sakaguchi

Citations in the corpus

• Turning 'sweet' on immunity: galectin–glycan interactions in immune tolerance and inflammation (2009, background): “However, these glycoproteins can either positively or negatively regulate cell susceptibility to galectin 1-induced apoptosis depending on their glycosylation statu”
• The Foxp3+ regulatory T cell: a jack of all trades, master of regulation (2008, background): “In this context, it is notable that the galectins also mediate cell death by a perforin- and granzyme-independent mechanism, which suggests a potential link between these two pathway”
• Protein-glycan interactions in the control of innate and adaptive immune responses (2008, background): “Treatment with galectin-1 suppresses chronic inflammation in several models of autoimmunity by skewing the balance of the immune response toward a T H 2 cytokine profil”