T helper 17 cell-mediated inflammation axis (Th17 axis)

The Th17 cell-mediated inflammation axis defines the range of interactions and signaling events driven by Th17 cells, a subset of CD4+ T helper lymphocytes characterized by the production of IL-17A, IL-17F, IL-21, IL-22, and GM-CSF. Th17 cell polarization is triggered by cytokines including IL-6, TGF-β, IL-21, and IL-23, and maintained by transcription factor RORγt. Th17 cells are central to immune defense against extracellular pathogens and promote inflammation by recruiting and activating neutrophils, macrophages, and other immune cells. Dysregulation of this axis contributes to chronic and autoimmune inflammatory diseases (such as psoriasis, rheumatoid arthritis, multiple sclerosis, and inflammatory bowel disease) and is implicated in neurodegenerative, cardiovascular, and some neoplastic diseases. Therapeutic drugs targeting key cytokines (IL-17A, IL-23) or their receptors have proven efficacy in these disorders, but carry risks associated with broad immune modulation[1][4][6][7]. For structured data extraction, individual molecules (such as "Interleukin-17A receptor" or "Retinoic acid-related orphan receptor gamma-T") should be preferred over the aggregate term "Th17 cell-mediated inflammation axis."

Other names

Th17 axisTh17 inflammatory pathwayTh17-mediated inflammationTh17 pathway

Neutralization of IL-17A or its receptor (prevents Th17-mediated inflammation) Blockade of IL-23 or its receptor (inhibits Th17 cell maturation and pathogenicity) Blockade of IL-6 receptor (limits Th17 cell differentiation)