IL-17 exhibits biphasic effects in tissue repair, promoting acute healing but exacerbating chronic fibrosis.

Tissue injury repair is a complex biological process involving tightly regulated inflammatory and regenerative phases. Dysregulation in this balance often leads to chronic inflammation, impaired healing, or excessive fibrosis, a major contributor to organ dysfunction in diseases like pulmonary fibrosis, cirrhosis, and inflammatory bowel disease. Interleukin-17 (IL-17) is a key pleiotropic cytokine, signaling through the IL-17R, known to influence the expression of inflammatory mediators, growth factors, and matrix metalloproteinases. While broadly recognized for its pro-inflammatory roles in autoimmune diseases, emerging evidence suggests IL-17 also plays a critical, often beneficial, role in acute tissue regeneration. However, the precise mechanisms governing this "double-edged sword" effect—where IL-17 promotes healing in some contexts but exacerbates pathology in others—remain poorly understood. A holistic framework systematically explaining this duality across diverse tissue environments is critically needed to develop targeted therapeutic interventions.