Abstract
CD4+ effector cells, based on cytokine production, nuclear receptors and signaling pathways, have been categorized into four subsets. T-helper-1 cells produce IFN-γ, 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.
Highlights
For more than 30 years T-helper (Th) cells have been divided by immunologists into two functional subsets: Thelper-1 (Th1) and T-helper-2 (Th2)
This cascade of events in turn results in the production of IL-4, IL-5, IL-13, IL-21 and IL-31, which are important for host defense against helminths and contribute to the pathogenesis of asthma and allergy [3,4,5,6,7]
For CAM practitioners, these findings strongly suggest that targeting signature cytokine expression by Th1 or Th2 cells, in addition to targeting Th17 cells and their associated cytokines and transcription factors, directly or indirectly, may be more efficacious for the treatment of inflammatory and autoimmune disorders including neuroinflammation and neuroautoimmunity
Summary
For more than 30 years T-helper (Th) cells have been divided by immunologists into two functional subsets: Thelper-1 (Th1) and T-helper-2 (Th2). Interleukin (IL)-12 activates STAT4 and drives naıve CD4+ T cells to become Th1 cells that produce interferon-gamma (INF-γ) These signals from IL-12 and IFN-γ by acting through STAT4 and STAT1, increase the expression of the transcription factor called T-bet, which promotes further production of IFN-γ and commitment to the Th1 cell lineage. By signals through STAT6, secrete IL-4 that induces naıve CD4+ T cells to become Th2 cells This leads to the expression of transcription factor GATA3. Th17 cells are important for host defense against extracellular bacteria and are involved in mediating autoimmune diseases [6, 14, 15] CAM researchers should be aware that the extent to which some aspects of T-cell subsets in humans are firmly fixed while others may change will continue to be the subject of intense investigation and future reports
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