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eCAM Advance Access published online on July 21, 2009

eCAM, doi:10.1093/ecam/nep063
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© The Author 2009. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org

The Role of Th17 in Neuroimmune Disorders: Target for CAM Therapy. Part II

Aristo Vojdani and Jama Lambert

Immunosciences Lab., Inc., Los Angeles, CA 90035, USA

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, {alpha}-lipoic acid, resveratrol and others for their patients with autoimmunities, in particular those with neuroinflammation and neurodegeneration.

Keywords: blood–brain barrier – cytokines – inflammatory response – probiotics


For reprints and all correspondence: Aristo Vojdani, Immunosciences Lab., Inc., 822 S. Robertson Boulevard, Suite 312, Los Angeles, CA 90035, USA. Tel: +1-310-657-1077; Fax: +1-310-657-1053; E-mail: drari{at}msn.com

Received November 28, 2008; accepted May 22, 2009


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