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Abstract
Decades of research went into understanding the role that Th1 autoreactive T-cells play in neuroinflammation. Here we describe another effector population, the IL-17-producing T-helper lineage (Th17), which drives the inflammatory process. Through the recruitment of inflammatory infiltration neutrophils and the activation of matrix metalloproteinases, IL-17, a cytokine secreted by Th17 cells, contributes to blood-brain barrier breakdown and the subsequent attraction of macrophages and monocytes into the nervous system. The entry of cells along with the local production of inflammatory cytokines leads to myelin and axonal damage. This activation of the inflammatory response system is induced by different pathogenic factors, such as gut bacterial endotoxins resulting in progressive neurodegeneration by Th17 cells. Through the understanding of the role of bacterial endotoxins and other pathogenic factors in the induction of autoimmune diseases by Th17 cells, CAM practitioners will be able to design CAM therapies targeting IL-17 activity. Targeted therapy can restore the integrity of the intestinal and blood-brain barriers using probiotics, N-acetyl-cysteine, α-lipoic acid, resveratrol and others for their patients with autoimmunities, in particular those with neuroinflammation and neurodegeneration.
Highlights
In the previous article, we established the differentiation of activated T-helper cells into T-helper-17 (Th17) and the pathogenic role of interleukin-17 (IL-17) in neuroimmune disorders
These results strongly suggest that the cells co-expressing IL-17, IL-22 and granzyme B through the action of IL-17 and IL22 play a significant role in the induction and breach in the blood-brain barrier (BBB) and the permeabilization of BBB to circulating CD4+ lymphocytes and soluble molecules resulting in CNS inflammation [37]
The assessment of Th1 and Th2 cytokines is used as a guide for intervention by some complementary and alternative medicine (CAM) practitioners in implementing therapeutic interventions, it is the T-helper-17 producing IL-17 which has emerged as the most pathogenic helper cell meriting possible CAM intervention
Summary
Decades of research went into understanding the role that Th1 autoreactive T-cells play in neuroinflammation. We describe another effector population, the IL-17-producing T-helper lineage (Th17), which drives the inflammatory process. The entry of cells along with the local production of inflammatory cytokines leads to myelin and axonal damage. This activation of the inflammatory response system is induced by different pathogenic factors, such as gut bacterial endotoxins resulting in progressive neurodegeneration by Th17 cells. Through the understanding of the role of bacterial endotoxins and other pathogenic factors in the induction of autoimmune diseases by Th17 cells, CAM practitioners will be able to design CAM therapies targeting IL-17 activity. Targeted therapy can restore the integrity of the intestinal and blood-brain barriers using probiotics, N-acetyl-cysteine, α-lipoic acid, resveratrol and others for their patients with autoimmunities, in particular those with neuroinflammation and neurodegeneration
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