IL-17A and IL-17F produced by Th17 cells play a central pathogenic role in several autoimmune conditions. Their primary effector mechanism on epithelial and stromal cells involves:
- A Activation of CD8+ cytotoxic T cells via IL-17R signaling to enhance MHC-I antigen presentation
- B Stimulation of IgE class switching in B cells via IL-17/STAT6 cross-talk
- C Induction of CXCL1, CXCL5, CXCL8, and G-CSF causing neutrophil recruitment and activation at sites of inflammation ✓
- D Promotion of M2 macrophage polarization via IL-17-induced arginase-1 upregulation
Explanation
IL-17A and IL-17F signal through the IL-17RA/IL-17RC heterodimeric receptor complex on epithelial cells, fibroblasts, and macrophages, activating NF-kB and C/EBPs to upregulate CXC chemokines (CXCL1, CXCL5, CXCL8/IL-8) and G-CSF. This cytokine program is the primary Th17 effector mechanism, driving potent neutrophilic inflammation — the hallmark of Th17-mediated diseases (psoriasis, ankylosing spondylitis, IBD). CD8+ T cell activation is mediated by IL-2 and TCR signaling, not IL-17R. IgE class switching is primarily driven by IL-4/IL-13 via STAT6. M2 macrophage polarization involves IL-4, IL-13, and IL-10.
Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.
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Written and medically reviewed by the StethoPrep medical team.