Galectin-1: A Jack-of-All-Trades in the Resolution of Acute and Chronic Inflammation
Галектин-1: универсальный регулятор разрешения острого и хронического воспаления
2017-11-20
SCID: 54.1/cz7mndvx
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Gal-1-glycan interactionsGalectin-1glycan-binding proteinsimmune cell regulationresolution of inflammation
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Abstract (AI)
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.
Key Findings
1
Galectin-1 broadly promotes resolution of acute and chronic inflammation by targeting multiple innate and adaptive immune cell types.
2
Galectin-1 functions as a resolution-associated molecular pattern and negative-regulatory checkpoint across inflammation, autoimmunity, allergy, pregnancy, cancer, and infection.
3
Galectin-1 regulates T-cell and B-cell responses by altering receptor clustering and signaling, thereby controlling immune-cell activation, differentiation, and survival.
4
In innate immunity, Galectin-1 suppresses proinflammatory cytokine synthesis, neutrophil trafficking, eosinophil migration and survival, and mast cell degranulation.
5
Therapeutic modulation of Galectin-1–glycan interactions may reduce cancer immunosuppression, strengthen antimicrobial immunity, or mitigate excessive inflammation, depending on the intervention.
Research Object
Galectin-1 (Gal-1) and its interactions with immune cells during acute and chronic inflammation
Research Subject
Gal-1-mediated anti-inflammatory and proresolving regulation of innate and adaptive immune-cell activation, trafficking, differentiation, survival, and signaling
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2017-11-20
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