Integration of lectin–glycan recognition systems and immune cell networks in CNS inflammation

Méndez-Huergo, Santiago P.; Maller, Sebastián M.; Farez, Mauricio; Mariño, Karina; Correale, Jorge; Rabinovich, Gabriel A.

doi:10.1016/j.cytogfr.2014.02.003

Cited by 26 publications

(13 citation statements)

References 97 publications

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“…However, administration of recombinant Gal-1 attenuated disease severity (34), suggesting different roles for endogenous versus exogenous Gal-1 in the regulation of testicular inflammation. Moreover, although a substantial increase in Gal-1 was reported during the peak of inflammation in other models (85), testis immunopathology was not associated with upregulation of this lectin (34). These results suggest contextdependent regulation of Gal-1 expression and function in the control of autoimmune inflammation.…”

Section: Gal-1 In Autoimmune Diseases: Resetting Tolerogenic Programsmentioning

confidence: 63%

“…By controlling the fate and signaling of T cells, DCs, and CNS immune populations, including microglia, astrocytes, and oligodendrocytes, Gal-1 influences the development, severity, and resolution of experimental autoimmune encephalomyelitis (EAE), a rodent model of multiple sclerosis (85). First reported in Lewis rats (86), Gal-1 reduced clinical signs of EAE through diverse mechanisms (85). Endogenous Gal-1 was selectively upregulated by tolerogenic stimuli, and its expression increased during the peak and resolution phases of EAE (27,30).…”

Section: Gal-1 In Autoimmune Diseases: Resetting Tolerogenic Programsmentioning

confidence: 99%

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Galectin-1: A Jack-of-All-Trades in the Resolution of Acute and Chronic Inflammation

Sundblad

Morosi

Geffner

et al. 2017

The Journal of Immunology

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158

136

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Regulatory signals provide negative input to immunological networks promoting resolution of acute and chronic inflammation. Galectin-1 (Gal-1), a member of a family of evolutionarily conserved glycan-binding proteins, displays broad anti-inflammatory and proresolving activities by targeting multiple immune cell types. Within the innate immune compartment, Gal-1 acts as a resolution-associated molecular pattern by counteracting the synthesis of proinflammatory cytokines, inhibiting neutrophil trafficking, targeting eosinophil migration and survival, and suppressing mast cell degranulation. Likewise, this lectin controls T cell and B cell compartments by modulating receptor clustering and signaling, thus serving as a negative-regulatory checkpoint that reprograms cellular activation, differentiation, and survival. In this review, we discuss the central role of Gal-1 in regulatory programs operating during acute inflammation, autoimmune diseases, allergic inflammation, pregnancy, cancer, and infection. Therapeutic strategies aimed at targeting Gal-1-glycan interactions will contribute to overcome cancer immunosuppression and reinforce antimicrobial immunity, whereas stimulation of Gal-1-driven immunoregulatory circuits will help to mitigate exuberant inflammation.

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Section: Gal-1 In Autoimmune Diseases: Resetting Tolerogenic Programsmentioning

confidence: 63%

Section: Gal-1 In Autoimmune Diseases: Resetting Tolerogenic Programsmentioning

confidence: 99%

Galectin-1: A Jack-of-All-Trades in the Resolution of Acute and Chronic Inflammation

Sundblad

Morosi

Geffner

et al. 2017

The Journal of Immunology

Self Cite

158

136

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show abstract

“…Galectins , a family of glycan-binding proteins, are currently considered key players in several programs that control maturation, activation, differentiation, polarization, trafficking, cytokine synthesis and viability of immune cell populations (Rabinovich and Toscano, 2009; Mendez-Huergo et al, 2014; Rabinovich and Conejo-García, 2016). By crosslinking specific glycoconjugates, different members of the galectin family (15 members identified to date) behave as either pro-inflammatory or anti-inflammatory agents, regulating the initiation, amplification and resolution of acute and chronic inflammatory responses (Rabinovich et al, 2002; Rubinstein et al, 2004).…”

Section: The Inflammatory Response and Its Resolutionmentioning

confidence: 99%

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

Kalinec

Lomberk

Urrutia

et al. 2017

Front. Cell. Neurosci.

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A significant number of studies support the idea that inflammatory responses are intimately associated with drug-, noise- and age-related hearing loss (DRHL, NRHL and ARHL). Consequently, several clinical strategies aimed at reducing auditory dysfunction by preventing inflammation are currently under intense scrutiny. Inflammation, however, is a normal adaptive response aimed at restoring tissue functionality and homeostasis after infection, tissue injury and even stress under sterile conditions, and suppressing it could have unintended negative consequences. Therefore, an appropriate approach to prevent or ameliorate DRHL, NRHL and ARHL should involve improving the resolution of the inflammatory process in the cochlea rather than inhibiting this phenomenon. The resolution of inflammation is not a passive response but rather an active, highly controlled and coordinated process. Inflammation by itself produces specialized pro-resolving mediators with critical functions, including essential fatty acid derivatives (lipoxins, resolvins, protectins and maresins), proteins and peptides such as annexin A1 and galectins, purines (adenosine), gaseous mediators (NO, H2S and CO), as well as neuromodulators like acetylcholine and netrin-1. In this review article, we describe recent advances in the understanding of the resolution phase of inflammation and highlight therapeutic strategies that might be useful in preventing inflammation-induced cochlear damage. In particular, we emphasize beneficial approaches that have been tested in pre-clinical models of inflammatory responses induced by recognized ototoxic drugs such as cisplatin and aminoglycoside antibiotics. Since these studies suggest that improving the resolution process could be useful for the prevention of inflammation-associated diseases in humans, we discuss the potential application of similar strategies to prevent or mitigate DRHL, NRHL and ARHL.

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“…Although underappreciated for many years, emerging observations suggest essential roles for glycan-binding proteins and their corresponding glycosylated ligands in different central nervous system (CNS) pathologies (Rabinovich and Croci, 2012;Mendez-Huergo et al, 2014). In previous studies, we reported the functional recovery of mice with spinal cord injury (SCI) following local treatment with galectin-1 (Gal-1), a highly conserved glycan-binding protein, through mechanisms involving interruption of Semaphorin3A (Sema3A)-driven inhibitory signals (Quinta et al, 2014b).…”

Section: Introductionmentioning

confidence: 99%

Ligand-mediated Galectin-1 endocytosis prevents intraneural H2O2 production promoting F-actin dynamics reactivation and axonal re-growth

Quintá

Wilson

Blidner

et al. 2016

Experimental Neurology

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Integration of lectin–glycan recognition systems and immune cell networks in CNS inflammation

Cited by 26 publications

References 97 publications

Galectin-1: A Jack-of-All-Trades in the Resolution of Acute and Chronic Inflammation

Galectin-1: A Jack-of-All-Trades in the Resolution of Acute and Chronic Inflammation

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

Ligand-mediated Galectin-1 endocytosis prevents intraneural H2O2 production promoting F-actin dynamics reactivation and axonal re-growth

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