IL-1β interacted with the IL-1 receptor on BM MyPs to stimulate the production of monocytes and neutrophils in obesity that upregulates IL-1β secretion from adipose tissue macrophages.69 Similarly, in aged mice, IL-1β, together with IL-6 and IL-1α, is increased in BM extracellular space.70 Chronic administration of IL-1β diminishes the self-renewal capacity of HSPCs.43 IL-1β secretion from BM macrophages, which is increased in aged mice, promotes myeloid-biased CD41+ HSCs.71 IL-1β and GM-CSF signaling in HSPCs explain increased myelopoiesis of β-glucan-induced trained immunity in mice.72 This evidence concerns the gene IL1B and obesity due to melanocortin 4 receptor deficiency.