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 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 Human adipose tissue-derived mesenchymal stem cells in Parkinson's disease：Inhibit T helper 17 cell differentiation and regulate immune balance towards a regulatory T cell phenotype

2020 ◽  
Author(s):  
Yong Bi ◽  
Huazheng Liang ◽  
Xiaobin Lin ◽  
Dehao Yang ◽  
Xiaowei Zhang ◽  
...  
Keyword(s):  
T Cells ◽  
Peripheral Blood ◽  
Th17 Cells ◽  
Mononuclear Cells ◽  
Inflammatory Responses ◽  
Neurodegenerative Disorder ◽  
Cell Phenotype ◽  
T Helper ◽  
T Helper 17 ◽  
Immune Balance

Abstract Parkinson's disease (PD), known as a neurodegenerative disorder, shows typical pathology of neuroinflammation, which might be the result of the imbalance between regulatory T cells (Treg) and T helper 17 (Th17) cells. The present study aimed to investigate the modulating effect of Ad-MSCs on peripheral blood mononuclear cells (PBMCs) derived from PD patients. CD4 + peripheral blood T cells were isolated and co-cultured with Ad-MSCs at a ratio of 4:1 under Th17 or Treg polarizing conditions, respectively, for 4 days. Our results showed that Ad-MSCs specifically inhibited the differentiation of IL-17-producing CD4 + T cells collected from PBMCs of PD patients evidenced by the decreased expression of RORγt- the key transcription factor for Th17 cells, IL-6R, and IL-23R. In the meantime, Ad-MSCs and induced a functional CD4 + CD25 + Foxp3 + T regulatory cell phenotype evidenced by the secretion of IL-10. Furthermore, levels of LIF protein and its receptor mRNA were significantly increased under both polarizing conditions. These findings suggest that the regulation of the Th17/Treg balance by Ad-MSCs was correlated with the increase in LIF secretion. Therefore, Ad-MSCs are an important player in ­modulating inflammatory responses and a potential therapeutics for PD patients.

scholarly journals Human adipose tissue-derived mesenchymal stem cells in Parkinson's disease：Inhibit T helper 17 cell differentiation and regulate immune balance towards a regulatory T cell phenotype

2020 ◽  
Author(s):  
Yong Bi ◽  
Xiaobin Lin ◽  
Huazheng Liang ◽  
Dehao Yang ◽  
Xiaowei Zhang ◽  
...  
Keyword(s):  
T Cells ◽  
Peripheral Blood ◽  
Th17 Cells ◽  
Mononuclear Cells ◽  
Inflammatory Responses ◽  
Neurodegenerative Disorder ◽  
Cell Phenotype ◽  
T Helper ◽  
T Helper 17 ◽  
Immune Balance

Abstract Parkinson's disease (PD), known as a neurodegenerative disorder, shows typical pathology of neuroinflammation, which might be the result of the imbalance between regulatory T cells (Treg) and T helper 17 (Th17) cells. The present study aimed to investigate the modulating effect of Ad-MSCs on peripheral blood mononuclear cells (PBMCs) derived from PD patients. CD4 + peripheral blood T cells were isolated and co-cultured with Ad-MSCs at a ratio of 4:1 under Th17 or Treg polarizing conditions, respectively, for 4 days. Our results showed that Ad-MSCs specifically inhibited the differentiation of IL-17-producing CD4 + T cells collected from PBMCs of PD patients evidenced by the decreased expression of RORγt- the key transcription factor for Th17 cells, IL-6R, and IL-23R. In the meantime, Ad-MSCs and induced a functional CD4 + CD25 + Foxp3 + T regulatory cell phenotype evidenced by the secretion of IL-10. Furthermore, levels of LIF protein and its receptor mRNA were significantly increased under both polarizing conditions. These findings suggest that the regulation of the Th17/Treg balance by Ad-MSCs was correlated with the increase in LIF secretion. Therefore, Ad-MSCs are an important player in ­modulating inflammatory responses and a potential therapeutics for PD patients.

scholarly journals Survival Proteins Encourage Human T Helper 17 Cells to Escape from Cell Death

Proceedings ◽  
2018 ◽  
Vol 2 (25) ◽  
pp. 1541
Author(s):  
Tuğçe Çimen ◽  
Ayten Nalbant
Keyword(s):  
T Cells ◽  
Western Blot ◽  
Peripheral Blood ◽  
Cd4 T Cells ◽  
Th17 Cells ◽  
Mononuclear Cells ◽  
Family Members ◽  
T Helper ◽  
T Helper 17 ◽  
Cell Lysate

IL-17 producing T helper 17 (Th17) cells are identified as a distinct subset of CD4+ T helper cells. They play a role in immune response. Abnormal regulation of Th17 cells can play a role in different type of pathologies such autoimmune diseases and cancer. The apoptotic and survival mechanisms of Th17 cells are not well known in different type of diseases. Therefore, the aim of the study was to investigate Bcl-2 family proteins to understand the regulation network of apoptosis in human Th17 cells. To do that, Peripheral blood (PB) were drawn from the healthy volunteers. Peripheral Blood Mononuclear Cells (PBMCs) were isolated from blood by Ficoll gradient isolation method. The naïve CD4+ T cells were isolated from PBMC. Sorted naive CD4+ T cells were cultured under Th17 polarizing conditions. Th17 cells were characterized by Flow cytometry. Cell lysates were obtained from negative controls and Th17 cells. Bcl-2 family members (Bik, BID and Puma) in Th17 cells were detected by western blot. Data showed that naive T cells were differentiated into Th17 cells. Then, cell lysate of this cells were used for western blot experiments. In the Th17 cell lysate, BH3 family members Bik and Puma were not detectable but Mcl-1 expression was increased. Overall data indicated that the pro-apoptotic BH3-only subgroup proteins Bik and Puma was not detectable, however anti-apoptotic Mcl-1 protein expression was increased.

scholarly journals Interleukin-12 Is the Optimum Cytokine To Expand Human Th17 Cells In Vitro

2009 ◽  
Vol 16 (6) ◽  
pp. 798-805 ◽  
Author(s):  
Soad Nady ◽  
James Ignatz-Hoover ◽  
Mohamed T. Shata
Keyword(s):  
T Cells ◽  
Peripheral Blood ◽  
Th17 Cells ◽  
Interleukin 12 ◽  
Interleukin 17 ◽  
Functional Evaluation ◽  
Optimum Conditions ◽  
T Helper ◽  
Ifn Γ

ABSTRACT Recently, a new lineage of CD4+ T cells in humans and in mice has been reported. This T helper cell secretes interleukin-17 (IL-17) and has been defined as T helper 17 (Th17). Th17 cells express the IL-23 receptor (IL-23R) and play an important pathogenic role in different inflammatory conditions. In this study, our aim was to characterize the optimum conditions for isolation and propagation of human peripheral blood Th17 cells in vitro and the optimum conditions for isolation of Th17 clones. To isolate Th17 cells, two steps were taken. Initially, we negatively isolated CD4+ T cells from peripheral blood mononuclear cells of a normal human blood donor. Then, we isolated the IL-23R+ cells from the CD4+ T cells. Functional studies revealed that CD4+ IL-23R+ cells could be stimulated ex vivo with anti-CD3/CD28 to secrete both IL-17 and gamma interferon (IFN-γ). Furthermore, we expanded the CD4+ IL-23R+ cells for 1 week in the presence of anti-CD3/CD28, irradiated autologous feeder cells, and different cytokines. Our data indicate that cytokine treatment increased the number of propagated cells 14- to 99-fold. Functional evaluation of the expanded number of CD4+ IL-23R+ cells in the presence of different cytokines with anti-CD3/CD28 revealed that all cytokines used (IL-2, IL-7, IL-12, IL-15, and IL-23) increased the amount of IFN-γ secreted by IL-23R+ CD4+ cells at different levels. Our results indicate that IL-7 plus IL-12 was the optimum combination of cytokines for the expansion of IL-23R+ CD4+ cells and the secretion of IFN-γ, while IL-12 preferentially stimulated these cells to secrete predominately IL-17.

scholarly journals Notch signaling pathway regulates CD4+CD25+CD127dim/− regulatory T cells and T helper 17 cells function in gastric cancer patients

2019 ◽  
Vol 39 (5) ◽  
Author(s):  
Lu Yang ◽  
Ke-Lei Zhao ◽  
Lei Qin ◽  
Dan-Xia Ji ◽  
Bin Zhang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
T Cells ◽  
Regulatory T Cells ◽  
Notch Signaling ◽  
Cancer Progression ◽  
Th17 Cells ◽  
Cellular Proliferation ◽  
Current Data ◽  
T Helper ◽  
T Helper 17

Abstract Regulatory T cells (Tregs) and T helper 17 (Th17) cells contribute to cancer progression and prognosis. However, regulatory factors associated with Tregs–Th17 balance were not completely understood. We previously demonstrated an immune-modulatory capacity by Notch signaling inactivation to reverse Tregs–Th17 disequilibrium in chronic hepatitis C. Thus, the aim of current study was to assess the role of Notch signaling in modulation Tregs and Th17 cells function in gastric cancer (GC) patients. A total of 51 GC patients and 18 normal controls (NCs) were enrolled. Notch1 and Notch2 mRNA expressions were semiquantified by real-time polymerase chain reaction. Tregs/Th17 percentages, transcriptional factors, and cytokines production were investigated in response to the stimulation of Notch signaling inhibitor DAPT. Both Notch1 and Notch2 mRNA expressions were elevated in GC tissues and peripheral bloods in GC patients. CD4+CD25+CD127dim/− Tregs and Th17 cells percentage was also elevated in GC patients compared with in NCs. DAPT treatment did not affect frequency of either circulating Tregs or Th17 cells, however, reduced FoxP3/RORγt mRNA expression and interleukin (IL)-35/IL-17 production in purified CD4+ T cells from GC patients. Moreover, blockade of Notch signaling also inhibited the suppressive function of purified CD4+CD25+CD127dim/− Tregs from GC patients, which presented as elevation of cellular proliferation and IL-35 secretion. The current data further provided mechanism underlying Tregs–Th17 balance in GC patients. The link between Notch signaling and Th cells might lead to a new therapeutic target for GC patients.

scholarly journals T Helper 17 Cells in Autoimmune Liver Diseases

2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Masanori Abe ◽  
Yoichi Hiasa ◽  
Morikazu Onji
Keyword(s):  
T Cells ◽  
Immune Responses ◽  
Autoimmune Diseases ◽  
Th17 Cells ◽  
Transforming Growth Factor ◽  
Treg Cells ◽  
Reciprocal Relationship ◽  
Th2 Cells ◽  
T Helper ◽  
T Helper 17

Many autoimmune diseases are driven by self-reactive T helper (Th) cells. A new population of effector CD4+T cells characterized by the secretion of interleukin (IL)-17, referred to as Th17 cells, has been demonstrated to be phenotypically, functionally, and developmentally distinct from Th1 and Th2 cells. Because the liver is known to be an important source of transforming growth factor-βand IL-6, which are cytokines that are crucial for Th17 differentiation, it is very likely that Th17 cells contribute to liver inflammation and autoimmunity. In contrast, another distinct subset of T cells, regulatory T cells (Treg), downregulate immune responses and play an important role in maintaining self-tolerance. In addition, there is a reciprocal relationship between Th17 cells and Tregs, in development and effector functions, and the balance between Th17 and Treg cells can affect the outcome of immune responses, particularly in autoimmune diseases. In this review, we will focus on the latest investigative findings related to Th17 cells in autoimmune liver disease.

Forkhead box P3-positive regulatory T-cells and interleukin 17-positive T-helper 17 cells in chronic inflammatory periodontal disease

2014 ◽  
Vol 49 (6) ◽  
pp. 817-826 ◽  
Author(s):  
V. P. B. Parachuru ◽  
D. E. Coates ◽  
T. J. Milne ◽  
H. M. Hussaini ◽  
A. M. Rich ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Periodontal Disease ◽  
Interleukin 17 ◽  
T Helper ◽  
T Helper 17 ◽  
T Helper 17 Cells ◽  
Forkhead Box P3 ◽  
Forkhead Box
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