Th17

Th17 refers to a subset of CD4+ T helper cells characterized by production of interleukin-17 family cytokines, notably IL-17A and IL-17F. The lineage is primarily defined by the transcription factor RORγt (RORC in humans) and the signaling through STAT3. Naive CD4+ T cells differentiate into Th17 cells in response to cytokines in lymphoid tissues; in mice, the combination of transforming growth factor beta (TGF-β) and interleukin-6 (IL-6) drives differentiation; in humans, TGF-β together with IL-6 or IL-1β, and IL-21 can support differentiation and expansion. IL-23 is not strictly required for initial differentiation but is critical for the stabilization, expansion, and pathogenic potential of Th17 cells.

Th17 cells contribute to host defense, especially at mucosal surfaces and in responses to extracellular bacteria and fungi such as Candida albicans. They secrete IL-17A, IL-17F, IL-22 and other effector molecules, promoting the production of chemokines (e.g., CXCL1, CXCL8) and recruitment of neutrophils, and inducing antimicrobial peptides from epithelial cells. However, Th17 responses are also linked to inflammatory and autoimmune diseases, including psoriasis, psoriatic arthritis, inflammatory bowel disease, multiple sclerosis, and rheumatoid arthritis, through excessive or dysregulated IL-17 signaling and interactions with innate immune cells.

Th17 cells display plasticity and can acquire Th1-like features under certain conditions, producing interferon-gamma in the presence of IL-12. This functional versatility underlies both protective roles and pathological inflammation. Therapeutic strategies have targeted the IL-17 axis in several autoimmune diseases, underscoring the clinical relevance of Th17 biology.