IL17F

Interleukin-17F (IL-17F) is a pro-inflammatory cytokine in the interleukin-17 (IL-17) family. It is produced by several cell types, including T helper 17 (Th17) cells, innate lymphoid cells, and epithelial or other stromal cells. IL-17F can form homodimers or heterodimers with IL-17A, and these complexes influence inflammatory responses in various tissues.

IL-17F signals through a receptor complex composed of IL-17RA and IL-17RC. Upon ligand binding, the adaptor protein Act1 is recruited, activating downstream pathways such as NF-κB and mitogen-activated protein kinases. This leads to transcription of inflammatory mediators, including chemokines like CXCL1, CXCL2, and CXCL8, as well as cytokines such as IL-6 and GM-CSF, which promote neutrophil recruitment and local inflammation.

In immunity, IL-17F contributes to mucosal defense and barrier integrity, particularly at epithelial surfaces. It often acts in concert with IL-17A to amplify responses to extracellular bacteria and fungi, helping coordinate innate and adaptive immunity in the gut, skin, and airways.

Clinically, IL-17F participates in several inflammatory disorders where IL-17 signaling is dysregulated. Elevated IL-17F–related activity has been reported in conditions such as psoriasis, psoriatic arthritis, inflammatory bowel disease, and some asthma phenotypes. Therapeutic strategies that block IL-17A and/or the IL-17 receptor can affect IL-17F signaling; dual IL-17A/F inhibitors (for example, bimekizumab) have shown efficacy in plaque psoriasis and psoriatic arthritis. Blocking IL-17 signaling can increase susceptibility to mucocutaneous candidiasis.

Ongoing research continues to define IL-17F–specific roles, its regulation, and potential as a biomarker or therapeutic target.