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

FEBS Lett. 2015 Nov 14;589(22):3407-18. doi: 10.1016/j.febslet.2015.08.037. Epub 2015 Sep 6.

Abstract

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.

Keywords: Galectin; Immunosuppression; M2-type macrophage; Myeloid-derived suppressor cell; Regulatory T cell; Tolerogenic dendritic cell.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Galectins / metabolism*
  • Humans
  • Immune System / cytology*
  • Immune System / immunology
  • Immune System / metabolism
  • Polysaccharides / metabolism*
  • Protein Binding

Substances

  • Galectins
  • Polysaccharides