T helper 17 cell response (Th17 response)

The T helper 17 cell response refers to the biological activity and inflammatory pathway mediated by T helper 17 (Th17) cells, a distinct lineage of CD4+ effector T cells. These cells are defined by their expression of the master transcription factor RORγt and the secretion of signature pro-inflammatory cytokines, including interleukin-17A (IL-17A), IL-17F, and IL-22 [PubMed: 18416897]. While the Th17 response is physiologically critical for host defense against extracellular bacteria and fungi at mucosal surfaces, its dysregulation is a major driver of chronic inflammatory and autoimmune pathologies [NIH: PMC3083110]. Therapeutic strategies frequently target this response by inhibiting the IL-23/IL-17 axis, either by neutralizing the cytokines themselves or by blocking their respective receptors [StatPearls: NBK553140]. Monoclonal antibodies such as secukinumab and guselkumab have revolutionized the treatment of Th17-mediated conditions like plaque psoriasis and ankylosing spondylitis by dampening this overactive immune signaling [Wikipedia: T helper 17 cell]. However, because this pathway is essential for mucosal integrity, pharmacological inhibition carries specific safety risks, most notably an increased susceptibility to Candida infections and the risk of worsening underlying inflammatory bowel disease [PubMed: 28882583].

Other names

Th17 pathwayIL-17/IL-23 axisT helper 17 cell mediated immunityInterleukin-17 signaling pathway

Neutralization of effector cytokines (IL-17A, IL-17F), blockade of cytokine receptors (IL-17RA), inhibition of upstream regulatory cytokines (IL-23), or antagonism of the master transcription factor RORγt.