Interleukin-17A pathway in CD4+ T cells (IL-17A pathway (CD4+))

The Interleukin-17A pathway in CD4+ T cells consists of the synthesis, secretion, and receptor-mediated signal transduction of IL-17A cytokine, primarily by Th17 cells and other CD4+ T cell subsets. Following antigen presentation and specific cytokine cues (IL-1β, IL-6, TGF-β, IL-21), naïve CD4+ T cells differentiate into Th17 cells, which produce IL-17A, IL-17F, and related cytokines. These cytokines engage IL-17RA/RC receptors on local or systemic immune cells, activating transcriptional programs predominantly through the Act1 adapter, JAK/STAT, and NF-κB pathways, leading to proinflammatory signaling, neutrophil recruitment, antimicrobial defense, degradation of extracellular matrix via MMPs, and modulation of cell death and survival. Dysregulated activation of this pathway drives the pathogenesis of a broad range of autoimmune, inflammatory, infectious, and cardiovascular diseases, making it a highly attractive therapeutic target with multiple currently approved monoclonal antibodies (e.g., secukinumab, brodalumab) and ongoing drug development.

Other names

IL-17 pathwayTh17 signaling pathwayIL-17A signaling in CD4+ T cellsInterleukin-17A/Interleukin-17F pathwayTh17 effector pathway

Monoclonal antibody blockade of IL-17A, IL-17F, or both. Antagonism of IL-17 receptor (IL-17RA/RC). Inhibition of upstream cytokines such as IL-23 to reduce IL-17 production. Reduction of inflammatory cytokine and chemokine production. Inhibition of JAK/STAT and NF-κB mediated signaling.