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Trends Mol Med. 2018 Apr;24(4):348-363. doi: 10.1016/j.molmed.2018.02.008. Epub 2018 Mar 16.

Untangling Galectin-Driven Regulatory Circuits in Autoimmune Inflammation.

Author information

1
Laboratorio de Inmunopatología, Instituto de Biología y Medicina Experimental (IBYME), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), C1428, Buenos Aires, Argentina; Equal contribution. Electronic address: m.toscano@ibyme.conicet.gov.ar.
2
Laboratorio de Inmunopatología, Instituto de Biología y Medicina Experimental (IBYME), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), C1428, Buenos Aires, Argentina; Equal contribution.
3
Laboratorio de Inmunopatología, Instituto de Biología y Medicina Experimental (IBYME), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), C1428, Buenos Aires, Argentina; Laboratorio de Glicómica Funcional y Molecular, Instituto de Biología y Medicina Experimental (IBYME), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET) C1428, Buenos Aires, Argentina.
4
Laboratorio de Inmunopatología, Instituto de Biología y Medicina Experimental (IBYME), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), C1428, Buenos Aires, Argentina; Departamento de Química Biológica, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, C1428, Buenos Aires, Argentina; Equal contribution. Electronic address: gabriel.r@ibyme.conicet.gov.ar.
5
Laboratorio de Glicómica Funcional y Molecular, Instituto de Biología y Medicina Experimental (IBYME), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET) C1428, Buenos Aires, Argentina; Equal contribution.

Abstract

Although progress has been made in understanding the mechanisms implicated in the pathogenesis of autoimmune inflammation, studies aimed at identifying the mediators of these pathways will be necessary to develop more selective therapies. Galectins, a family of glycan-binding proteins, play central roles in immune cell homeostasis. Whereas some members of this family trigger regulatory programs that promote resolution of inflammation, others contribute to perpetuate autoimmune processes. We discuss the roles of endogenous galectins and their specific glycosylated ligands in shaping autoimmune responses by fueling, extinguishing, or rewiring immune circuits. Understanding the relevance of galectin-glycan interactions in autoimmune inflammation could help to uncover novel pathways of tolerance breakdown, define molecular signatures for patient stratification and therapy responses, and open new avenues for immune intervention.

KEYWORDS:

autoimmunity; chronic inflammation; galectins; glycans; immunoregulation

PMID:
29555188
DOI:
10.1016/j.molmed.2018.02.008
[Indexed for MEDLINE]

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