T helper 17 cytokine network (Th17 pathway)

The T helper 17 (Th17) cytokine network is a specialized immune signaling axis primarily defined by the production of pro-inflammatory cytokines, including IL-17A, IL-17F, IL-21, and IL-22, by Th17 cells [1]. This network is orchestrated by the master transcription factor RORγt and is critically dependent on Interleukin-23 (IL-23) for the maintenance and expansion of the Th17 phenotype [2]. Biologically, the Th17 axis plays a vital role in mucosal immunity and host defense against extracellular pathogens, particularly fungi and bacteria [3]. However, dysregulation or overactivation of this pathway is a central driver in the pathogenesis of several autoimmune and chronic inflammatory disorders, such as plaque psoriasis, psoriatic arthritis, and ankylosing spondylitis [1,4]. Therapeutic strategies targeting this network involve monoclonal antibodies that either neutralize specific cytokines (e.g., IL-17A, IL-17F, or IL-23) or block their respective receptors (e.g., IL-17RA) [4,5]. These interventions have significantly improved clinical outcomes for patients with moderate-to-severe inflammatory diseases. Despite their efficacy, targeting this network requires careful monitoring for safety concerns, including an increased risk of mucocutaneous candidiasis and the potential for exacerbating underlying inflammatory bowel disease [3,6].

Other names

IL-17/IL-23 axisTh17 pathwayIL-17 signaling pathwayT helper 17 pathway

Neutralization of pro-inflammatory cytokines (IL-17A, IL-17F, IL-23) or blockade of their receptors (IL-17RA) to inhibit downstream inflammatory signaling pathways [4,5].