Finally, coactin-like protein and gut-derived lipid metabolites such as 12,13-diHOME illustrate how perturbed lipid-handling pathways can skew macrophages toward either a prostaglandin D2–CRTH2-driven pro-inflammatory state or an IL-1β-high CD206-low phenotype that dampens IFN responses and increases the risk of childhood allergy and asthma (Pan et al., 2025; Lin et al., 2024). This evidence concerns the gene IL1B and asthma.