Although progress has been made in understanding the mechanisms implicated in the pathogenesis of autoimmune inflammation, studies aimed at identifying the mediators of these pathways will be necessary to develop more selective therapies. Galectins, a family of glycan-binding proteins, play central roles in immune cell homeostasis. Whereas some members of this family trigger regulatory programs that promote resolution of inflammation, others contribute to perpetuate autoimmune processes. We discuss the roles of endogenous galectins and their specific glycosylated ligands in shaping autoimmune responses by fueling, extinguishing, or rewiring immune circuits. Understanding the relevance of galectin–glycan interactions in autoimmune inflammation could help to uncover novel pathways of tolerance breakdown, define molecular signatures for patient stratification and therapy responses, and open new avenues for immune intervention.

尽管在了解自身免疫性炎症的发病机理方面已取得进展，但旨在鉴定这些途径的介质的研究对于开发更具选择性的疗法将是必要的。半乳凝素是一种聚糖结合蛋白家族，在免疫细胞稳态中起着核心作用。该家族的某些成员触发了促进炎症消退的调节程序，而其他成员则促进了永久性自身免疫过程。我们讨论了内源性半乳糖凝集素及其特定糖基化配体在通过加重，扑灭或重新连接免疫回路来塑造自身免疫应答中的作用。了解半乳糖凝集素-聚糖相互作用在自身免疫性炎症中的相关性可能有助于发现耐受性破坏的新途径，