Abstract
It has been reported that degenerated and herniated lumbar intervertebral discs show high expression of IL-17, suggesting that local immune reactions occur in patients with low back pain. While clinical sample analyses from different laboratories confirm this, it is not deeply not known on how IL-17 is induced in the pathology and their interactions with other inflammatory responses. This conscience review organizes current laboratory findings on this topic and present trajectory for full understanding on the role of IL-17 in pathology of intervertebral disc disease.
Highlights
The intervertebral disc (IVD) consists of an outer fibrocartilaginous annulus fibrosus (AF) that surrounds a gel-like nucleus pulposus (NP)
When Shamji et al analyzed IVD degeneration (IDD) and LDH patients’ samples, the percentage of CD4+ lymphocytes and CD68+ macrophages were significantly higher in NP of both IDD and LDH compared with healthy IVD, and the expression of IL-4, IL-6, IL-12, IL-17, and IFNγ were significantly higher in NP of LDH compared with IDD; notably, IL-17A was elevated. These findings suggest that T helper 17 (Th17) differentiation and activation inducing IL-17A production mediate the inflammatory processes underlying IVD pathology (Shamji et al, 2010)
Peroxisome proliferator-activated receptor γ (PPAR-γ), which inhibits the NF-κB signal pathway, decreased in degenerative IVD tissues compared with nondegenerated tissues, and a peroxisome proliferator-activated receptor γ (PPAR-γ) agonist downregulated the production of IL-1β, CCL20, COX-2, PGE-2, matrix metalloprotease (MMP)-13, and ADAMTS-7 induced by IL-17A along with tumor necrosis factor-α (TNFα) in NP cells (Liu et al, 2019)
Summary
The intervertebral disc (IVD) consists of an outer fibrocartilaginous annulus fibrosus (AF) that surrounds a gel-like nucleus pulposus (NP). The analysis of the correlation between chemokines and inflammatory cytokine gene expression in humans reported a significant correlation between CCR6 and IL-17A expression both in IVD tissues and blood samples (Singh et al, 2008; Hiyama et al, 2021) These studies indicate that IL-17Aproducing cells might participate in the degeneration of disc tissues via an interaction with the CCL20/CCR6 system in vivo. Peroxisome proliferator-activated receptor γ (PPAR-γ), which inhibits the NF-κB signal pathway, decreased in degenerative IVD tissues compared with nondegenerated tissues, and a PPAR-γ agonist downregulated the production of IL-1β, CCL20, COX-2, PGE-2, MMP-13, and ADAMTS-7 induced by IL-17A along with TNFα in NP cells (Liu et al, 2019) Overall, these studies indicate that IL-17A synergize with TNFα to stimulate the NFκB signaling pathway and contributes to the production of cytokines, chemokines, and extracellular matrix-degrading factors in IVD (Figure 2)
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