Interleukin-1 alpha (IL-1α), encoded by the IL1A gene, is a critical pleiotropic cytokine that plays a central role in the initiation and propagation of inflammatory responses and the regulation of innate immunity ^[1]. Primarily expressed by monocytes, macrophages, dendritic cells, and epithelial cells in response to cellular stress, damage, or pathogen recognition, IL-1α can exert its effects both as a precursor within the cell or upon release through non-classical secretory pathways. This cytokine triggers a cascade of downstream signaling events, influencing diverse biological processes including fever induction, acute-phase protein synthesis, and the activation and recruitment of immune cells to sites of inflammation ^[2]. While essential for host defense and tissue repair, dysregulation of IL1A expression and signaling is implicated in the pathogenesis of various diseases, including rheumatoid arthritis, ankylosing spondylitis, chronic periodontitis, and potentially osteoarthritis and certain cancers, highlighting its significance as a potential therapeutic target ^[3].

The B6-hIL1A mice are a humanized model constructed by replacing the mouse Il1a gene sequence and the 3' UTR region in situ with the corresponding sequence of the human IL1A gene. The B6-hIL1A mice can be used for the research of diseases such as rheumatoid arthritis, ankylosing spondylitis, chronic periodontitis, Alzheimer's disease (AD) and related vascular dementia, diabetes mellitus, systemic sclerosis, autoimmune encephalomyelitis, and cerebral infarction, and for IL1A-targeted drugs development.