Autologous nucleus pulposus primes T cells to develop into interleukin‐4‐producing effector cells: An experimental study on the autoimmune properties of nucleus pulposus

Abstract

An autoimmune response to herniated nucleus pulposus has been proposed to constitute a pathophysiologic mechanism for inducing sciatica based on the fact that nucleus pulposus under normal conditions is excluded from the development of immunological tolerance. The manifestation of an autoimmune response comprises different steps starting with antigen capture, continuing with activation of T helper (T H ) cells and ending with production of autoantibodies. Activated T H cells differentiate into either T H 1 cells, predominately producing proinflammatory cytokines such as interferon g (IFNg) or a T H 2 subset mainly producing anti-inflammatory cytokines such as interleukin-4 (IL-4).

Primary immune system responders to nucleus pulposus cells: evidence for immune response in disc herniation

“…Macrophages and NK cells, but not T cells, were detected, although the presence of T and B cells in isolated human herniated discs and in experimental porcine models has been previously reported (Geiss et al, 2007). Our results suggest an early immunological response after normal NP tissues were exposed to the immune system.…”

“…Nachemson (1969) reported decreased pH levels within and around a herniated lumbar disc and speculated that sciatica was caused by an inflammatory reaction surrounding the nerve root. Subsequently, various inflammatory chemical factors secreted from herniated NP, including tumor necrosis factor (TNF)-α (Weiler et al, 2005;Le Maitre et al, 2007), interleukin (IL)-1β (Le Maitre et al, 2007) and nitric oxide (NO) (Katsuno et al, 2008), have been implicated as causes of sciatica (McCarron et al, 1987;Geiss et al, 2007). Further, the production of matrix metalloproteinases (MMPs) has been implicated in the resorption of the herniated NP (Doita et al, 2001).…”

“…The expression of , and interferon (IFN)-γ suggests Th1 lymphocyte activation (Kang et al, 1996;Burke et al, 2002;Park et al, 2002). Geiss et al placed autologous porcine NP in subcutaneous titanium chambers and observed the infiltration of activated T and B cells (Geiss et al, 2007), including IL-4-producing Th2 cells and γδ T cells (Geiss et al, 2008). These results indicate both innate and acquired immune responses to the NP.…”

Presence of various autoantibodies demonstrated by autoimmune target test in the sera of patients with degenerated and herniated intervertebral disc: Comment on the article by Shamji et al

“…Previous reports have stated that herniated nucleus pulposus could be related to autoimmune response (4,5). The nucleus pulposus is an immune-privileged site because it is avascular and is thus excluded from immune surveillance.…”

Effects of degenerative autologous nucleus pulposus on the lumbar sympathetic trunk: Sympathetic inflammation in rats

“…Given the location of the sympathetic nerve trunk being immediately anterior to the lumbar spine, it is logical that these nerves might be affected by NP leakage caused by anterior disc herniation. Nonetheless, anterior herniation is seldom considered as one of the sources of sympathetic nerve-related syndromes, despite many studies having confirmed a sympathetic pain pathway [8][9][10][11] . Therefore, there is a possibility that anterior herniation of the lumbar discs may induce sympathetic inflammatory pain.…”