LANCL2 (lanthionine synthetase C-like 2) is a broadly expressed immunometabolic signaling protein that regulates inflammatory and metabolic responses through ligand-dependent intracellular signaling mechanisms
[1][2]. Mechanistically, LANCL2 functions as a receptor and signaling mediator for abscisic acid (ABA), promoting cAMP-dependent pathways, calcium signaling, and downstream immunoregulatory responses that influence cellular metabolism and immune activation
[3][4]. Activation of the LANCL2 pathway is linked to PPARγ-mediated transcriptional programs, regulation of inflammatory cytokine production, and enhancement of regulatory immune cell responses, thereby connecting metabolic control with immune homeostasis
[1][5]. In disease models, LANCL2 signaling suppresses intestinal inflammation, supports regulatory macrophage and T-cell differentiation, and ameliorates experimental colitis through modulation of TNF-α, IFN-γ, IL-10, and related immune pathways
[5][6]. LANCL2 has also been implicated in adipogenesis and insulin-sensitizing processes, highlighting its relevance to chronic metabolic disorders and diabetes-associated inflammation
[1][2]. Compared with the structurally related isoform LANCL1, which has been characterized primarily through structural and glutathione-binding studies, LANCL2 is distinguished by its established role in ABA-dependent signaling and immunometabolic regulation
[3][7]. For experimental applications, small-molecule LANCL2 agonists including NSC61610, BT-11, and related compounds have been used to investigate anti-inflammatory mechanisms and therapeutic responses in inflammatory bowel disease and other immune-mediated disease models
[4][6].