IL-17

Interleukin-17 (IL-17) is a pro-inflammatory cytokine primarily produced by Th17 cells and other immune subsets, functioning as a key mediator in host defense and tissue inflammation^[1][2][3]. IL-17 signals through the IL-17 receptor (IL-17R) complex, activating downstream NF-κB, MAPK, and JNK pathways, thereby promoting transcription of inflammatory mediators^[1][4][5]. Mechanistically, IL-17 isoforms exhibit distinct expression patterns, with IL-17F predominating in enthesis tissue and peripheral CD4⁺ T cells, whereas IL-17A is less abundant^[6]. In disease models, IL-17 contributes to psoriasis, psoriatic arthritis, necrotizing enterocolitis, and ischemic brain injury by amplifying local inflammation and modulating neutrophil and microglial responses^{[2][7][8][9][10][11]}. Compared with related cytokines such as IL-17A and IL-17F, IL-17RA serves as a shared receptor subunit critical for signaling of multiple IL-17 isoforms except IL-17D, highlighting functional specificity among isoforms^[4]. Pharmacologically, IL-17 inhibitors including secukinumab, ixekizumab, and brodalumab demonstrate potent anti-inflammatory effects in moderate-to-severe psoriasis and psoriatic arthritis, whereas A2a receptor agonists and PPARγ agonists modulate IL-17 production for experimental applications^{[7][2][12][13]}. These therapeutic strategies exploit mechanistic insights into isoform-specific signaling and receptor interactions, providing rational frameworks for preclinical and clinical research^[14][15][16].