scholarly journals The regulatory role of interferon-γ producing gamma delta T cells via the suppression of T helper 17 cell activity in bleomycin-induced pulmonary fibrosis

2016 ◽  
Vol 185 (3) ◽  
pp. 348-360 ◽  
Author(s):  
S. Segawa ◽  
D. Goto ◽  
A. Iizuka ◽  
S. Kaneko ◽  
M. Yokosawa ◽  
...  
Keyword(s):  
T Cells ◽  
Pulmonary Fibrosis ◽  
Cell Activity ◽  
Interferon Γ ◽  
Gamma Delta T Cells ◽  
T Helper ◽  
Gamma Delta ◽  
T Helper 17 ◽  
T Helper 17 Cell

scholarly journals The Role of Th17 in Neuroimmune Disorders: Target for CAM Therapy. Part I

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Aristo Vojdani ◽  
Jama Lambert
Keyword(s):  
Autoimmune Diseases ◽  
Signaling Pathways ◽  
Allergic Inflammation ◽  
T Helper ◽  
T Helper 1 ◽  
T Helper 17 ◽  
Effector Cells ◽  
Pathogenic Factors ◽  
T Helper 17 Cell

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-βand 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.

scholarly journals Circulating and gut-resident human Th17 cells express CD161 and promote intestinal inflammation

2009 ◽  
Vol 206 (3) ◽  
pp. 525-534 ◽  
Author(s):  
Melanie A. Kleinschek ◽  
Katia Boniface ◽  
Svetlana Sadekova ◽  
Jeff Grein ◽  
Erin E. Murphy ◽  
...  
Keyword(s):  
T Cells ◽  
Cd4 T Cells ◽  
Th17 Cells ◽  
Intestinal Inflammation ◽  
Interferon Γ ◽  
Intestinal Cells ◽  
T Helper ◽  
T Helper 17 ◽  
Inflammatory Stimuli ◽  
Cc Chemokine Receptor 6

The C-type lectin-like receptor CD161, which has recently been described to promote T cell expansion, is expressed on a discrete subset of human CD4 T cells. The function of such cells, however, has remained elusive. We now demonstrate that CD161+ CD4 T cells comprise a circulating and gut-resident T helper 17 (Th17) cell population. During Crohn's disease (CD), these CD161+ cells display an activated Th17 phenotype, as indicated by increased expression of interleukin (IL)-17, IL-22, and IL-23 receptor. CD161+ CD4 T cells from CD patients readily produce IL-17 and interferon γ upon stimulation with IL-23, whereas, in healthy subjects, priming by additional inflammatory stimuli such as IL-1β was required to enable IL-23–induced cytokine release. Circulating CD161+ Th17 cells are imprinted for gut homing, as indicated by high levels of CC chemokine receptor 6 and integrin β7 expression. Supporting their colitogenic phenotype, CD161+ Th17 cells were found in increased numbers in the inflammatory infiltrate of CD lesions and induced expression of inflammatory mediators by intestinal cells. Our data identify CD161+ CD4 T cells as a resting Th17 pool that can be activated by IL-23 and mediate destructive tissue inflammation.

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