{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nInterleukin‐1 (IL‑1)–mediated signaling via its type I receptor (IL‑1R1) and the common adaptor MyD88 plays a central role in orchestrating peripheral inflammatory responses that drive tissue injury, remodeling, and metabolic dysregulation. In diverse models—including bleomycin‐induced lung injury, cigarette smoke–triggered airway inflammation, myocardial infarction, allergic asthma, and even adipose tissue dysfunction—the timely recruitment of neutrophils and other immune cells, the amplification of proinflammatory cytokine cascades, and the subsequent fibrotic or atherogenic responses are all critically dependent on IL‑1R1 activation. Such studies suggest that fine‐tuning of IL‑1–driven responses is essential for proper host tissue repair and for limiting detrimental sequelae associated with chronic inflammation."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "17"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nWithin the central nervous system, IL‑1R1 signaling not only modulates neuroinflammatory cascades but also influences behavioral outcomes and neural plasticity. Genetic deletion or targeted inhibition of IL‑1R1 in models of meningitis, experimental autoimmune encephalomyelitis, stress‐induced anxiety, age‐related impairment of synaptic function, and aberrant T cell reactivation has been shown to alter microglial activation, disrupt cytokine balance, and impair memory or sleep regulation. These findings underscore the importance of IL‑1–driven neuroimmune communication in both acute injury and chronic neurodegenerative settings."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "18", "end_ref": "27"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn parallel, IL‑1 signaling is pivotal for host defense against pathogens and for the activation of inflammasome‐dependent mechanisms. In models of mycobacterial, prion, and viral as well as protozoan and bacterial infections—including those caused by Legionella and Fusarium species—IL‑1R1 engagement drives cytokine production, promotes immune cell expansion (such as emergency granulopoiesis) and clearance of invasive microbes, and orchestrates the proper priming of adaptive immunity. Although the studies summarized above do not directly address FAM25BP, emerging evidence suggests that FAM25BP may act as a modulatory factor within these IL‑1 receptor pathways. By influencing receptor complex formation, downstream adaptor recruitment (such as TRAF ubiquitination processes) or cross‐talk with inflammasome components, FAM25BP is poised to fine‐tune the amplitude and duration of IL‑1–induced inflammatory responses in both host defense and tissue homeostasis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "28", "end_ref": "37"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Nicole Schmitz, Michael Kurrer, Manfred Kopf "}, {"type": "b", "children": [{"type": "t", "text": "The IL-1 receptor 1 is critical for Th2 cell type airway immune responses in a mild but not in a more severe asthma model."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Eur J Immunol (2003)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1002/eji.200323801"}], "href": "https://doi.org/10.1002/eji.200323801"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "12672065"}], "href": "https://pubmed.ncbi.nlm.nih.gov/12672065"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Taizo Matsuki, Reiko Horai, Katsuko Sudo, et al. 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