Mouse IL-17A (Interleukin-17A) is a pro-inflammatory cytokine belonging to the IL-17 family that plays a critical role in host defense and immune-mediated inflammation in mice (Mus musculus). IL-17A is produced primarily by Th17 CD4⁺ T cells, as well as by γδ T cells, innate lymphoid cells (ILC3s), and other activated lymphocyte populations in response to microbial infection and inflammatory stimulation. It acts on epithelial, endothelial, and stromal cells to induce expression of pro-inflammatory cytokines (such as IL-6 and TNF-α), chemokines (including CXCL1 and CXCL2), and antimicrobial peptides, thereby promoting neutrophil recruitment and strengthening mucosal barrier immunity. In healthy mice, basal IL-17A expression is generally low but increases significantly during bacterial and fungal infections, particularly at mucosal surfaces. Dysregulated IL-17A signaling has been implicated in numerous experimental disease models, including experimental autoimmune encephalomyelitis (EAE), collagen-induced arthritis, psoriasis-like dermatitis, inflammatory bowel disease, and asthma. In biomedical research, mouse IL-17A is widely studied as a central mediator of Th17-driven immunity, neutrophilic inflammation, and autoimmune pathology, and serves as a key target for investigating immunomodulatory therapies in translational disease models.