scholarly journals Effects of IL-17 on Epidermal Development

2021 ◽  
Author(s):  
Emi Sato ◽  
Shinichi Imafuku
Keyword(s):  
Th17 Cells ◽  
Terminal Differentiation ◽  
Lymphoid Cells ◽  
The Other ◽  
Interleukin 17 ◽  
T Helper 17 ◽  
Epidermal Structure ◽  
Biological Responses ◽  
Group 3 ◽  
Epidermal Development

Immunotherapies targeting interleukin 17 (IL-17) have a strong effect on plaque psoriasis. However, many previous studies on IL-17 focused only on the T-helper 17 (Th17) immune response, and a few studies have reported that IL-17A may affect psoriatic epidermal structure. IL-17 includes six family members, namely IL-17A–F, which are involved in a wide variety of biological responses. IL-17A is produced mainly by Th17 cells or group 3 innate lymphoid cells (ILC3), while IL-17C is locally produced by epithelial cells, such as keratinocytes. In contrast to IL-17C, which is locally produced in various cells such as keratinocytes, it is predicted that IL-17A, which is produced by limited cells and has systemic effects, has different roles in epidermal development. For example, several research studies have shown that IL-17A affects terminal differentiation of epidermis by suppressing the expression of filaggrin or loricrin in keratinocytes. On the other hand, IL-17C, which is produced by keratinocytes themselves, does not have as strong as an effect on epidermal development as IL-17A. In this chapter, we summarized the effects of IL-17A and other IL-17 members on epidermal development and their comprehensive roles based on previously reported papers.

scholarly journals Pivotal Roles of T-Helper 17-Related Cytokines, IL-17, IL-22, and IL-23, in Inflammatory Diseases

2013 ◽  
Vol 2013 ◽  
pp. 1-13 ◽  
Author(s):  
Ning Qu ◽  
Mingli Xu ◽  
Izuru Mizoguchi ◽  
Jun-ichi Furusawa ◽  
Kotaro Kaneko ◽  
...  
Keyword(s):  
Th17 Cell ◽  
Th17 Cells ◽  
Functional Role ◽  
Inflammatory Diseases ◽  
Interleukin 17 ◽  
T Helper ◽  
T Helper 17 ◽  
Autoimmune Encephalomyelitis ◽  
Experimental Autoimmune

T-helper 17 (Th17) cells are characterized by producing interleukin-17 (IL-17, also called IL-17A), IL-17F, IL-21, and IL-22 and potentially TNF-α and IL-6 upon certain stimulation. IL-23, which promotes Th17 cell development, as well as IL-17 and IL-22 produced by the Th17 cells plays essential roles in various inflammatory diseases, such as experimental autoimmune encephalomyelitis, rheumatoid arthritis, colitis, and Concanavalin A-induced hepatitis. In this review, we summarize the characteristics of the functional role of Th17 cells, with particular focus on the Th17 cell-related cytokines such as IL-17, IL-22, and IL-23, in mouse models and human inflammatory diseases.

scholarly journals Fenofibrate Inhibited the Differentiation of T Helper 17 CellsIn Vitro

PPAR Research ◽  
2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Zhou Zhou ◽  
Weiliang Sun ◽  
Ying Liang ◽  
Yanxiang Gao ◽  
Wei Kong ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Autoimmune Diseases ◽  
Th17 Cells ◽  
Transforming Growth Factor ◽  
Inflammatory Diseases ◽  
Lipid Lowering ◽  
Interleukin 17 ◽  
T Helper ◽  
T Helper 17 ◽  
Th17 Differentiation

Uncontrolled activity of T cells mediates autoimmune and inflammatory diseases such as multiple sclerosis, inflammatory bowel diseases, rheumatoid arthritis, type 1 diabetes, and atherosclerosis. Recent findings suggest that enhanced activity of interleukin-17 (IL-17) producing T helper 17 cells (Th17 cells) plays an important role in autoimmune diseases and inflammatory diseases. Previous papers have revealed that a lipid-lowering synthetic ligand of peroxisome proliferator-activated receptorα(PPARα), fenofibrate, alleviates both atherosclerosis and a few nonlipid-associated autoimmune diseases such as autoimmune colitis and multiple sclerosis. However, the link between fenofibrate and Th17 cells is lacking. In the present study, we hypothesized that fenofibrate inhibited the differentiation of Th17 cells. Our results showed that fenofibrate inhibited transforming growth factor-β(TGF-β) and IL-6-induced differentiation of Th17 cellsin vitro. However, other PPARαligands such as WY14643, GW7647 and bezafibrate did not show any effect on Th17 differentiation, indicating that this effect of fenofibrate might be PPARαindependent. Furthermore, our data showed that fenofibrate reduced IL-21 production and STAT3 activation, a critical signal in the Th17 differentiation. Thus, by ameliorating the differentiation of Th17 cells, fenofibrate might be beneficial for autoimmunity and inflammatory diseases.

Abstract 075: Proinflammatory T Helper 17 Cells as an Indicator of Hypertension

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Seungbum Kim ◽  
Vermali Rodriguez ◽  
Carl J Pepine ◽  
Mohan K Raizada
Keyword(s):  
T Cells ◽  
Progenitor Cells ◽  
Th17 Cells ◽  
Human Study ◽  
Interleukin 17 ◽  
Ang Ii ◽  
T Helper ◽  
T Helper 17 ◽  
Important Indicator ◽  
Hematopoietic Stem

Objectives: T cells and interleukin 17 (IL17) have been shown to be critical in the development of hypertension (HTN). This implicates a significant role of IL17 producing T helper 17 (Th17) cells in HTN. Thus, the objective of our study was to investigate if Th17 cell levels in the peripheral blood (PB) and the bone marrow (BM) are correlated with blood pressure. Methods: Saline or Ang II was chronically infused into C57BL6 mice (1000ng Ang II/kg/min using osmotic pumps) for 3 weeks. This resulted in an increase in MAP of 45±10 mmHg. BM and PB from saline and Ang II-treated mice were analyzed using FACS. A parallel human study was conducted using blood samples obtained from hypertensive patients (n = 8, systolic BP ≥125 mmHg) and normotensive subjects (n = 10, systolic BP <125 mmHg). FACS analysis was used to examine changes in the inflammatory cells levels in these patients. Results: We observed 87% and 36% increases in both Sca-1 + c-Kit + Lin - hematopoietic stem cell (HSC; 0.23±0.04% vs. 0.43±0.05%) and Sca-1 + c-Kit - Lin - lymphoid progenitors (10.8±1.1% vs. 14.7±2.9%) in the BM of Ang II infused mice. These are upstream stem/progenitor cells for T cells. This was associated with 30% and 190% increases in CD4 + IL17 + Th17 cells in the BM and PB (1.20±0.09% vs. 1.61±0.19 % and 4.8±2.0 % vs. 14.7±3.8 % respectively) in the Ang II infused mice. Importantly, there were 58% and 206% increases of angiotensin II type 1 receptor (AT1R) expressing CD4 + T cells in the BM and PB of Ang II HTN mice (0.40±0.04 % vs. 0.63±0.14 % and 1.1±0.2 % vs 3.4±1.1 % respectively) and ~ 85% of these cells were also positive for IL-17. Consistent with mouse data, analysis of PB showed a 470% increase of Th17 cells in HTN patients (0.48±0.18 % vs 2.72±1.2%). Conclusions: We observed (i) Increased hematopoietic stem/progenitor cells in Ang II HTN mice; (ii) increased Th17 cells in both HTN mice and humans and (iii) the majority of AT1R expressing CD4 + T cells was Th17 cells. Taken together, these observations indicate that Th17 cells may be an important indicator of those destined to develop HTN and suggest that these cells may represent a novel therapeutic target.

scholarly journals Superantigenic Staphylococcus aureus Stimulates Production of Interleukin-17 from Memory but Not Naive T Cells

2009 ◽  
Vol 78 (1) ◽  
pp. 381-386 ◽  
Author(s):  
Ulrika Islander ◽  
Annica Andersson ◽  
Erika Lindberg ◽  
Ingegerd Adlerberth ◽  
Agnes E. Wold ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
T Cells ◽  
Th17 Cells ◽  
Mononuclear Cells ◽  
Memory T Cells ◽  
Inflammatory Diseases ◽  
Commensal Bacteria ◽  
Interleukin 17 ◽  
T Helper ◽  
T Helper 17

ABSTRACT T-helper 17 (Th17) cells are characterized by their production of interleukin-17 (IL-17) and have a role in the protection against infections and in certain inflammatory diseases. Humans who lack Th17 cells are more susceptible to Staphylococcus aureus infections compared to individuals having Th17 cells. S. aureus is part of the commensal skin microflora and also colonize the infant gut. To investigate whether UV-killed S. aureus would be more capable of inducing IL-17 than other commensal bacteria, we stimulated mononuclear cells from adults, infants, and newborns with various gram-positive and gram-negative commensal bacteria. IL-17 was produced from adult memory Th17 cells after stimulation with superantigen-producing S. aureus but not nonsuperantigenic S. aureus or other common commensal gut bacteria. Cells from newborns were poor IL-17 producers after stimulation with S. aureus, whereas in some cases IL-17 was secreted from cells isolated from infants at the age of 4 and 18 months. These results suggest that superantigenic S. aureus are particularly efficient in stimulating IL-17 production and that the cytokine is produced from memory T cells.

scholarly journals The Role of IL-17 and Related Cytokines in Inflammatory Autoimmune Diseases

2017 ◽  
Vol 2017 ◽  
pp. 1-11 ◽  
Author(s):  
Taku Kuwabara ◽  
Fumio Ishikawa ◽  
Motonari Kondo ◽  
Terutaka Kakiuchi
Keyword(s):  
T Cells ◽  
Autoimmune Diseases ◽  
Chronic Inflammation ◽  
Th17 Cells ◽  
Lymphoid Cells ◽  
Interleukin 17 ◽  
Human Rheumatoid Arthritis ◽  
Functional Understanding ◽  
Bacteria And Fungi

Interleukin-17 (IL-17) induces the production of granulocyte colony-stimulating factor (G-CSF) and chemokines such as CXCL1 and CXCL2 and is a cytokine that acts as an inflammation mediator. During infection, IL-17 is needed to eliminate extracellular bacteria and fungi, by inducing antimicrobial peptides such as defensin. This cytokine also plays an important role in chronic inflammation that occurs during the pathogenesis of autoimmune diseases and allergies such as human rheumatoid arthritis (RA) for which a mouse model of collagen-induced arthritis (CIA) is available. In autoimmune diseases such as RA and multiple sclerosis (MS), IL-17 is produced by helper T (Th) cells that are stimulated by IL-1βand IL-6 derived from phagocytes such as macrophages and from tissue cells. IL-17 contributes to various lesions that are produced by Th17 cells, one subset of helper T cells, and byγδT cells and innate lymphoid cells. It strongly contributes to autoimmune diseases that are accompanied by chronic inflammation. Thus, a functional understanding of Th17 cells is extremely important. In this review, we highlight the roles of cytokines that promote the development and maintenance of pathogenic Th17 cells in autoimmune diseases.

scholarly journals Transient inhibition of ROR-γt therapeutically limits intestinal inflammation by reducing TH17 cells and preserving group 3 innate lymphoid cells

2016 ◽  
Vol 22 (3) ◽  
pp. 319-323 ◽  
Author(s):  
David R Withers ◽  
Matthew R Hepworth ◽  
Xinxin Wang ◽  
Emma C Mackley ◽  
Emily E Halford ◽  
...  
Keyword(s):  
Th17 Cells ◽  
Intestinal Inflammation ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Group 3

scholarly journals The nuclear receptor REV-ERBα modulates Th17 cell-mediated autoimmune disease

2019 ◽  
Vol 116 (37) ◽  
pp. 18528-18536 ◽  
Author(s):  
Christina Chang ◽  
Chin-San Loo ◽  
Xuan Zhao ◽  
Laura A. Solt ◽  
Yuqiong Liang ◽  
...  
Keyword(s):  
Autoimmune Diseases ◽  
Nuclear Receptor ◽  
Th17 Cells ◽  
Inflammatory Responses ◽  
Retinoic Acid Receptor ◽  
Nuclear Hormone Receptor ◽  
Interleukin 17 ◽  
Orphan Nuclear Receptor ◽  
T Helper 17 ◽  
Autoimmune Encephalomyelitis

T helper 17 (Th17) cells produce interleukin-17 (IL-17) cytokines and drive inflammatory responses in autoimmune diseases such as multiple sclerosis. The differentiation of Th17 cells is dependent on the retinoic acid receptor-related orphan nuclear receptor RORγt. Here, we identify REV-ERBα (encoded byNr1d1), a member of the nuclear hormone receptor family, as a transcriptional repressor that antagonizes RORγt function in Th17 cells. REV-ERBα binds to ROR response elements (RORE) in Th17 cells and inhibits the expression of RORγt-dependent genes includingIl17aandIl17f. Furthermore, elevated REV-ERBα expression or treatment with a synthetic REV-ERB agonist significantly delays the onset and impedes the progression of experimental autoimmune encephalomyelitis (EAE). These results suggest that modulating REV-ERBα activity may be used to manipulate Th17 cells in autoimmune diseases.

scholarly journals Interleukin 17 and senescent cells regulate the foreign body response to synthetic material implants in mice and humans

2020 ◽  
Vol 12 (539) ◽  
pp. eaax3799 ◽  
Author(s):  
Liam Chung ◽  
David R. Maestas ◽  
Andriana Lebid ◽  
Ashlie Mageau ◽  
Gedge D. Rosson ◽  
...  
Keyword(s):  
T Cells ◽  
Foreign Body ◽  
Foreign Body Response ◽  
The Body ◽  
Lymphoid Cells ◽  
Interleukin 17 ◽  
Synthetic Material ◽  
T Helper 17 ◽  
Synthetic Materials ◽  
Body Response

Medical devices and implants made of synthetic materials can induce an immune-mediated process when implanted in the body called the foreign body response, which results in formation of a fibrous capsule around the implant. To explore the immune and stromal connections underpinning the foreign body response, we analyzed fibrotic capsules surrounding surgically excised human breast implants from 12 individuals. We found increased numbers of interleukin 17 (IL17)–producing γδ+ T cells and CD4+ T helper 17 (TH17) cells as well as senescent stromal cells in the fibrotic capsules. Further analysis in a murine model demonstrated an early innate IL17 response to implanted synthetic material (polycaprolactone) particles that was mediated by innate lymphoid cells and γδ+ T cells. This was followed by a chronic adaptive CD4+ TH17 cell response that was antigen dependent. Synthetic materials with varying chemical and physical properties implanted either in injured muscle or subcutaneously induced similar IL17 responses in mice. Mice deficient in IL17 signaling established that IL17 was required for the fibrotic response to implanted synthetic materials and the development of p16INK4a senescent cells. IL6 produced by senescent cells was sufficient for the induction of IL17 expression in T cells. Treatment with a senolytic agent (navitoclax) that killed senescent cells reduced IL17 expression and fibrosis in the mouse implant model. Discovery of a feed-forward loop between the TH17 immune response and the senescence response to implanted synthetic materials introduces new targets for therapeutic intervention in the foreign body response.

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