Interleukin-10 receptor subunit alpha (IL-10RA) (IL-10RA)

Interleukin-10 receptor subunit alpha (IL-10RA) is the high-affinity, ligand-binding component of the IL-10 receptor complex, primarily expressed on hematopoietic cells such as macrophages, monocytes, and T cells [1, 2, 10]. On inflammatory macrophages, IL-10RA plays a pivotal role in the resolution of inflammation by mediating the anti-inflammatory effects of IL-10 through the JAK1/STAT3 signaling pathway [2, 6, 7]. Activation of this receptor leads to the suppression of pro-inflammatory cytokines, including TNF-alpha, IL-1, and IL-6, and promotes the polarization of macrophages toward a regulatory, anti-inflammatory phenotype [3, 13, 15]. Genetic deficiencies or loss-of-function mutations in IL-10RA are strongly associated with severe, early-onset inflammatory bowel disease (IBD), underscoring its essential function in maintaining immune homeostasis [2, 17, 18]. Therapeutically, IL-10RA is targeted by recombinant IL-10 (Ilodecakin) and engineered agonists like Pegilodecakin to treat autoimmune disorders and certain cancers, where it can also modulate the tumor microenvironment [3, 8, 9, 11]. However, therapeutic use is often limited by pleiotropic effects and safety concerns such as anemia and thrombocytopenia [9, 12].

Other names

IL10RACD210CD210aIL-10R1HIL-10RCDw210aInterleukin-10 receptor subunit 1

Agonism of the IL-10 receptor complex to activate the JAK1/STAT3 pathway, leading to the suppression of pro-inflammatory cytokine production and induction of anti-inflammatory gene expression in macrophages.