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eCAM Advance Access published online on July 21, 2009
eCAM, doi:10.1093/ecam/nep062
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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 I

Aristo Vojdani and Jama Lambert

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

CD4+ effector cells, based on cytokine production, nuclear receptors and signaling pathways, have been categorized into four subsets. T-helper-1 cells produce IFN-{gamma}, TNF-β, lymphotoxin and IL-10; T-helper-2 cells produce IL-4, IL-5, IL-10, IL-13, IL-21 and IL-31; T-helper-3, or regulatory T-cells, produce IL-10, TGF-β and IL-35; and the recently discovered T-helper-17 cell produces IL-17, IL-17A, IL-17F, IL-21, IL-26 and CCL20. By producing IL-17 and other signaling molecules, Th17 contributes to the pathogenesis of multiple autoimmune diseases including allergic inflammation, rheumatoid arthritis, autoimmune gastritis, inflammatory bowel disease, psoriasis and multiple sclerosis. In this article, we review the differential regulation of inflammation in different tissues with a major emphasis on enhancement of neuroinflammation by local production of IL-17 in the brain. By understanding the role of pathogenic factors in the induction of autoimmune diseases by Th17 cells, CAM practitioners will be able to design CAM therapies targeting Th17 and associated cytokine activities and signaling pathways to repair the intestinal and blood–brain barriers for their patients with autoimmunities, in particular, those with neuroinflammation and neurodegeneration.

Keywords: antibodies – autoimmune response – cytokines – effectors – lymphocytes

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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