Re‐wiring regulatory cell networks in immunity by galectin–glycan interactions

Abstract

Edited by Wilhelm JustKeywords: Galectin Regulatory T cell Tolerogenic dendritic cell M2-type macrophage Myeloid-derived suppressor cell Immunosuppression a b s t r a c tPrograms 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, myeloidderived 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.

TRIMs and Galectins Globally Cooperate and TRIM16 and Galectin-3 Co-direct Autophagy in Endomembrane Damage Homeostasis

“…This work shows that TRIMs (Reymond et al, 2001) and Galectins (Arthur et al, 2015; Blidner et al, 2015; de Waard et al, 1976; Nabi et al, 2015) interact and that the TRIM16-Galectin-3 system organizes autophagic response to endomembrane damage. TRIM16 controls ubiquitination of damaged compartments, and regulates the core autophagy regulators ULK1, Beclin 1, and ATG16L1, which confer localized autophagic sequestration of damaged lysosomes (Maejima et al, 2013).…”

Resolution of Cochlear Inflammation: Novel Target for Preventing or Ameliorating Drug-, Noise- and Age-related Hearing Loss

“…Thus, they are able to stimulate different signaling cascades associated with inflammation (Norling et al, 2009; Rabinovich and Toscano, 2009; Blidner et al, 2015) and regulate the activity of immune cells by controlling the function of relevant glycosylated receptors.…”

Glycobiology simplified: diverse roles of glycan recognition in inflammation

“…However, they are transported across the plasma membrane (by nonclassic mechanisms) into the local extracellular milieu, where they bind to glycans bearing b-linked galactose residues, including galactose-terminated, branched, N-linked glycans and poly-LacNAc termini (Fig. Their physiologic effects are striking and broad, and excellent reviews provide more depth than can be included here [83][84][85][86]. In the immune system, galectins are expressed by many immune cells, including activated macrophages, dendritic cells, B cells, and T cells.…”

“…10). In these models, galectin-1 administration is accompanied by T cell apoptosis, a loss of Th1 and Th17 cells, a skewing toward Th2-type cytokines and expansion of Foxp3 + T regulatory cells [7,85]. In some contexts, galectin-1 is immunosuppressive and anti-inflammatory.…”