Re-wiring regulatory cell networks in immunity by galectin-glycan interactions.

FEBS Lett

Laboratory of Immunopathology and Functional Glycomics, Institute of Biology and Experimental Medicine (IBYME), CONICET, C1428 Buenos Aires, Argentina; School of Exact and Natural Sciences, University of Buenos Aires, C1428 Buenos Aires, Argentina. Electronic address:

Published: November 2015

Programs that control immune cell homeostasis are orchestrated through the coordinated action of a number of regulatory cell populations, including regulatory T cells, regulatory B cells, myeloid-derived suppressor cells, alternatively-activated macrophages and tolerogenic dendritic cells. These regulatory cell populations can prevent harmful inflammation following completion of protective responses and thwart the development of autoimmune pathology. However, they also have a detrimental role in cancer by favoring escape from immune surveillance. One of the hallmarks of regulatory cells is their remarkable plasticity as they can be positively or negatively modulated by a plethora of cytokines, growth factors and co-stimulatory signals that tailor their differentiation, stability and survival. Here we focus on the emerging roles of galectins, a family of highly conserved glycan-binding proteins in regulating the fate and function of regulatory immune cell populations, both of lymphoid and myeloid origins. Given the broad distribution of circulating and tissue-specific galectins, understanding the relevance of lectin-glycan interactions in shaping regulatory cell compartments will contribute to the design of novel therapeutic strategies aimed at modulating their function in a broad range of immunological disorders.

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http://dx.doi.org/10.1016/j.febslet.2015.08.037DOI Listing

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