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 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 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 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 Effect of IL-34 on T helper 17 cell proliferation and IL-17 secretion by peripheral blood mononuclear cells from rheumatoid arthritis patients

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Xin Li ◽  
Yimeng Lei ◽  
Ziyu Gao ◽  
Bei Zhang ◽  
Liping Xia ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Transcription Factor ◽  
Peripheral Blood ◽  
Th17 Cells ◽  
Mononuclear Cells ◽  
Treg Cells ◽  
T Helper ◽  
T Helper 17 ◽  
Peripheral Blood Mononuclear ◽  
Blood Mononuclear Cells

AbstractInterleukin (IL)-34 is a new pro-inflammatory cytokine with elevated expression in rheumatoid arthritis (RA) patients. Our previous study showed that the frequency of T helper 17 (Th17) cells was also elevated in RA patients. Our study aimed to determine the effects of IL-34 on the proliferation, transcription factor expression and cytokine secretion of different subgroups of CD4 + T cells [Th1, Th2, Th17 and regulatory T (Treg) cells] in RA patients. Peripheral blood mononuclear cells (PBMCs) were isolated from the peripheral blood of 10 RA patients and stimulated with different concentrations of recombinant human (rh) IL-34 (0, 25, 50 and 100 ng/ml). Flow cytometry was used to determine the frequencies of the 4 subgroups of CD4 + T cells. Reverse transcription-PCR, western blotting and enzyme-linked immunosorbent assays were used to determine the mRNA and protein expression levels of transcription factors and cytokines. As a result, the frequency of Th17 cells was obviously increased under IL-34 stimulation. Moreover, the expression of the transcription factor retinoic acid-related orphan receptor (ROR-γt) and secretion of IL-17 by PBMCs were increased by stimulation with IL-34. However, there were no effects of IL-34 on transcription factors or cytokine secretion in Th1, Th2 and Treg cells. In conclusion, IL-34 can improve the proliferation of Th17 cells and expression of IL-17 in RA patients.

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.

Aberrant peripheral blood CD4+ CD25+ FOXP3+ regulatory T cells/T helper-17 number is associated with the outcome of patients with lymphoma

2020 ◽  
Vol 69 (9) ◽  
pp. 1917-1928 ◽  
Author(s):  
Mehdi Dehghani ◽  
Mehdi Kalani ◽  
Hossein Golmoghaddam ◽  
Mani Ramzi ◽  
Nargess Arandi
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Peripheral Blood ◽  
T Helper ◽  
T Helper 17

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.

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