scholarly journals Acute Effect of Repeated Sprint and Aerobic Endurance Training on Foxp3+ Regulatory T Cells and Cytokine Levels

2021 ◽  
Author(s):  
Orkun Akkoç ◽  
Deniz Genç ◽  
Hakan Özel ◽  
Recep Fatih Kayhan ◽  
Muazzez Gökalp ◽  
...  
Keyword(s):  
Immune System ◽  
Endurance Training ◽  
T Regulatory Cells ◽  
Acute Effect ◽  
Wilcoxon Test ◽  
Regulatory Cells ◽  
Distance Runners ◽  
Tnf Α ◽  
Before And After ◽  
Ifn Γ

Objective: The aim of our study was to investigate the acute effect of repeated sprints and aerobic endurance training on Foxp3+ T regulatory cells and cytokines. Materials and Methods: The study population consisted of 16 sprinters and 16 long distance runners. Each subject was divided into his/her own branch as sprinting and distance training. Within the scope of the study, the height, body weight, sporting age, Foxp3+ T regulatory cells and cytokine values of subjects were recorded. Immunity subparameters were compared in venous blood samples taken before and after training. The Wilcoxon test was used to compare the values before and after training with level of statistical significance accepted as p<0.05. Results: A statistically significant change was not observed for Foxp3+ T regulatory cells before and after training in sprinter (p=0.47) and distance runners (p=0.52). Sprinters had increased IL-2 (p=0.00), IL-4 (p=0.00), IL-10 (p=0.02), IL-17 (p=0.000) and TNF-α (p=0.000), decreased IL-6 (p=0.000) and unchanged IFN-γ levels (p=0.81). Distance runners had increased IL-4 (p=0.000), IL-10 (p=0.000), IL-17 levels (p<0.00), decreased TNF-α (p=0.00), IL-2 (p=0.05) and unchanged IFN-γ (p=0.15) and IL-6 (p=0.15). Conclusion: Immune system is affected by the intensity and type of exercise. It can be said that anaerobic exercises like sprinting with high intensity supress the immune system more severely.

scholarly journals Phosphoantigen-activated Vγ2Vδ2 T cells antagonize IL-2–induced CD4+CD25+Foxp3+ T regulatory cells in mycobacterial infection

Blood ◽  
2009 ◽  
Vol 113 (4) ◽  
pp. 837-845 ◽  
Author(s):  
Guangming Gong ◽  
Lingyun Shao ◽  
Yunqi Wang ◽  
Crystal Y. Chen ◽  
Dan Huang ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Treatment Regimen ◽  
T Regulatory Cells ◽  
Mycobacterial Infection ◽  
T Cell Subsets ◽  
Regulatory Cells ◽  
Ifn Γ ◽  
Vγ2vδ2 T Cells

Abstract Although Foxp3+ T regulatory cells (Tregs) are well documented for their ability to suppress various immune cells, T-cell subsets capable of counteracting Tregs have not been demonstrated. Here, we assessed phosphoantigen-activated Vγ2Vδ2 T cells for the ability to interplay with Tregs in the context of mycobacterial infection. A short-term IL-2 treatment regimen induced marked expansion of CD4+CD25+Foxp3+ T cells and subsequent suppression of mycobacterium-driven increases in numbers of Vγ2Vδ2 T cells. Surprisingly, activation of Vγ2Vδ2 T cells by adding phosphoantigen Picostim to the IL-2 treatment regimen down-regulated IL-2–induced expansion of CD4+CD25+Foxp3+ T cells. Consistently, in vitro activation of Vγ2Vδ2 T cells by phosphoantigen plus IL-2 down-regulated IL-2–induced expansion of CD4+CD25+Foxp3+ T cells. Interestingly, anti–IFN-γ–neutralizing antibody, not anti–TGF-β or anti–IL-4, reduced the ability of activated Vγ2Vδ2 T cells to down-regulate Tregs, suggesting that autocrine IFN-γ and its network contributed to Vγ2Vδ2 T cells' antagonizing effects. Furthermore, activation of Vγ2Vδ2 T cells by Picostim plus IL-2 treatment appeared to reverse Treg-driven suppression of immune responses of phosphoantigen-specific IFNγ+ or perforin+ Vγ2Vδ2 T cells and PPD-specific IFNγ+αβ T cells. Thus, phos-phoantigen activation of Vγ2Vδ2 T cells antagonizes IL-2–induced expansion of Tregs and subsequent suppression of Ag-specific antimicrobial T-cell responses in mycobacterial infection.

scholarly journals SA-4-1BBL Costimulation Inhibits Conversion of Conventional CD4+ T Cells into CD4+FoxP3+ T Regulatory Cells by Production of IFN-γ

PLoS ONE ◽  
2012 ◽  
Vol 7 (8) ◽  
pp. e42459 ◽  
Author(s):  
Shravan Madireddi ◽  
Rich-Henry Schabowsky ◽  
Abhishek K. Srivastava ◽  
Rajesh K. Sharma ◽  
Esma S. Yolcu ◽  
...  
Keyword(s):  
T Cells ◽  
Cd4 T Cells ◽  
T Regulatory Cells ◽  
Regulatory Cells ◽  
Ifn Γ

Endogenous IL-β Selectively Converts T Regulatory Cells Into IL-17 Producers During Antigen Stimulation

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 586-586
Author(s):  
Lequn Li ◽  
Jin sub Kim ◽  
Vassiliki A Boussiotis
Keyword(s):  
T Cells ◽  
T Regulatory Cells ◽  
Neutralizing Antibody ◽  
Treg Cells ◽  
Conversion Process ◽  
Regulatory Cells ◽  
Antigen Stimulation ◽  
Tnf Α ◽  
Treg Population

Abstract Abstract 586 A major challenge of the immune system is to fight pathogens and tumor antigens while preserving tolerance to self-antigen. T regulatory cells (Treg) are critical extrinsic regulators of immune tolerance and maintenance of lymphoid homeostasis. Recently it was determined that, when used as cell-based immunosuppressive therapy, Treg have a potent effect in preventing GvHD in patients undergoing allogeneic stem cell transplantation. However, several studies suggest that the Treg phenotype is not at end stage of differentiation. Treg can express and produce effector cytokines including IFN-γ and IL-17 under certain conditions, particularly in the context of inflammatory milieu, suggesting that Treg may convert into inflammatory mediators. IL-1β and TNF-α are critical inflammatory cytokines that have been implicated in GvHD. The precise role and the mechanism(s) via which these cytokines may affect development of GvHD remain unclear. In the presence study, we sought to determine whether IL-1β and TNF-α regulate the properties of Treg and specifically whether these cytokines affect Treg expansion and/or conversion into IL-17 producing cells. CD4+CD25+Treg cells were isolated from B6 mice and were stimulated with anti-CD3-plus-anti-CD28 mAbs in the presence of either media, IL-1β or TNF-α. Addition of either cytokine induced Treg proliferation as determined by CFSE. Assessment of intracellular IL-17 expression by flow cytometry and IL-17 production by ELISA revealed that IL-1β but not TNF-α induced conversion of Treg into IL-17 producing cells, suggesting that conversion was mediated via pathways distinct from those that regulate cell cycle progression. To evaluate conversion of Treg to IL-17 producers during antigen stimulation and to determine the role of IL-1β in this process, we used neutral culture conditions in which no exogenous cytokines were supplied. Treg cells isolated from Foxp3GFP-KI mouse were added to cultures of naive conventional CD4+ T cells (Tc) in the presence of APC and anti-CD3 mAb. We found that these conditions preferentially induced conversion of Treg to IL-17 producing cells. To determine the role of IL-1β in this conversion process, we used IL-1β neutralizing antibody. Addition of anti-IL-1β neutralizing antibody reduced IL-17 production to almost undetectable levels. Because it has exogenous IL-6 can induce IL-17 production by both Treg and Tc, we evaluated whether endogenous IL-6 was involved in the conversion of Treg into IL-17 producing cells in our system. Addition of a combination of IL-6 neutralizing and IL-6 receptor blocking antibodies did not affect IL-17 production, suggesting that the conversion process of Treg into IL-17 producing cells was dependent on endogenous IL-1β rather than IL-6. To determine whether IL-1β was mandatory for this process, we used T cells from IL-1R deficient mice. Individual culture of IL−1R−/− Tc or IL-1R−/− Treg with wild type (wt) APC and co-culture of IL-1R−/− Tc and IL-1R−/− Treg with wt APC did not result in detectable IL-17 production. Similarly, no IL-17 production was observed when wt instead of IL-1R−/− Tc were used. In contrast, substitution of IL-1R−/− Treg with wt Treg resulted in abundant IL-17 production. To investigate the in vivo biological relevance of our findings we adoptively transferred Treg cells from either congenic B6.PL mice or IL-1R1−/− mice into IL-1R1−/− recipients, which were then immunized with KLH in IFA. Three days after immunization both IL-1R−/− Treg and IL-1R−/− Tc cells were incapable of producing detectable levels of IL-17 or expressing RORγt, the key transcriptional factor of IL-17. In contrast, a significant percentage of IL-17 and RORγt positive cells were detected within the adoptively transferred Thy1.1+ Treg population. Mechanistic analysis revealed that IL-1β induced activation of p38 and JNK in Treg and addition of pharmacologic inhibitors specific for these MAPKs abrogated IL-17 production. Our studies reveal that although Treg have primarily immunosuppressive functions they may also facilitate pro-inflammatory responses as they can be converted into IL-17 producing cells by IL-1β. These observations may have significant implications on clinical strategies that employ Treg for control of GvHD and suggest that further intervention might be required to prevent attainment of pro-inflammatory properties by Treg while maintaining their suppressive function. Disclosures: No relevant conflicts of interest to declare.

Interferon β-1b effects on cytokine mRNA in peripheral mononuclear cells in multiple sclerosis

1996 ◽  
Vol 1 (5) ◽  
pp. 262-269 ◽  
Author(s):  
PV Byskosh ◽  
AT Reder
Keyword(s):  
Multiple Sclerosis ◽  
Mononuclear Cells ◽  
Mrna Levels ◽  
Cytokine Mrna ◽  
Serum Triglycerides ◽  
Tnf Α ◽  
Before And After ◽  
Peripheral Mononuclear Cells ◽  
Ifn Γ ◽  
Polymerase Chain

IFN-β reduces the number and severity of exacerbations of multiple sclerosis (MS), presumably by modifying immune regulation. We used semiquantitative polymerase chain reaction (RT-PCR) to measure mRNA levels for cytokines before and after IFN β-1b therapy. mRNA was extracted from mononuclear cells of nine healthy controls and 31 patients with MS. Before therapy, IL-10 and leukemia inhibitory factor (UF) mRNA levels were elevated in stable MS compared to active MS. Twenty four hours after IFN β-1b treatment, mRNA levels for IL-1, IL-2, IL-4, IL-6, IL-10, IL-12, IL-13, IFN-γ, TNF-α and UF had not changed. At 1 week, TNF-α mRNA increased and IL-10 and UF mRNA rose in 75% of patients. IL-2, IL-4, IL-12, IL-13 and IFN-γ did not change. At 3 months, cytokine mRNA returned to baseline levels. mRNA for the IFN-induced antiviral enzyme, 2, 5-OAS, rose by 24 h, peaked at 1 week, and remained elevated thereafter. Serum triglycerides and liver enzymes rose after therapy. Increased SGPT at 3 months correlated with TNF-α mRNA levels, suggesting that cytokines may cause some side effects of IFN β-1b. Baseline cytokine mRNA levels reflect disease activity, but the therapeutic effect of IFN β-1b does not appear to be explained by changes in cytokine mRNA levels.

scholarly journals Immunosuppression factors under various pathologies

2011 ◽  
Vol 10 (4) ◽  
pp. 103-111
Author(s):  
Ye. G. Churina ◽  
V. V. Novitsky ◽  
O. I. Urazova
Keyword(s):  
Immune Response ◽  
Immune System ◽  
Direct Contact ◽  
Endocrine System ◽  
Recent Time ◽  
Regulatory Cells ◽  
Component Process ◽  
Suppressive Function ◽  
Neoplastic Processes ◽  
Ifn Γ

Until recent time it has seemed obvious that suppressive function in the immune system is provided by one subpopulation of Tlymphocytes-suppressors. At present it is usually considered that regulatory cells (T-reg) are key cells-suppressors of the immune response. There exist two main mechanisms of T-reg immunosuppression realization: direct (when there is direct contact between cells) and distant (cytokine-dependent). For suppression of the immune response Т-reg cells produce cytokines with suppression activity: TGF-β, IL-10, IFN-γ, IL-35. Meanwhile the increasing number of facts indicates that suppression of the immune response is a multi-component process. A considerable role in suppression of the immune response is assigned to the endocrine system. However, immunosuppression mechanisms under infection, neoplastic processes and the influence of xenobiotics on the organism are not completely clear.

scholarly journals Sex differences in morphofunctional changes in the immune system in Wistar rats of different age groups with experimental endotoxinemia

2020 ◽  
pp. 65-73
Author(s):  
Anna M. Kosyreva ◽  
Olga V. Makarova
Keyword(s):  
Gender Differences ◽  
Sex Differences ◽  
Immune System ◽  
Peripheral Blood ◽  
Wistar Rats ◽  
Ex Vivo ◽  
Age Groups ◽  
Mature Adult ◽  
Tnf Α ◽  
Ifn Γ

Objective. The aim was revealing gender differences in morphological and functional changes of lymphoid organs (thymus and spleen), changes of cytokine production and subpopulation composition of peripheral blood lymphocytes in Wistar rats of three age groups with endotoxemia. Materials and methods. We used male and female Wistar rats of three age groups: newborns, prepubertal and sexually mature adult rats. A day after the injection of 15 mg/kg of O26:B6 E. coli lipopolysaccharide (LPS), the volume fraction of the functional zones of the thymus and spleen, the number of AnnexinV + apoptotically dying cells in the thymus, the relative and absolute number of lymphocyte subpopulations (CD3+CD4+, CD3+CD8a+, CD4+CD25+Foxp3+, CD3-CD45R+) in peripheral blood and ex vivo production of IL-2, IL-4, IFN-γ and TNF-α were estimated. Results. Sex differences in the response of the immune system after the LPS injection in different age periods are expressed differently: in the neonatal period, there is immunosuppression in females (decrease in the ex vivo production of IL-2, TNF-α and IFN-γ), and there is activation of pro-inflammatory reactions in males (increase in ex vivo production of IL-2 and TNF-α). As compared with other age periods at prepubertal age, LPS-induced immunological disorders are more pronounced, and gender differences are minimal and related only to the number of T-regulatory and B-lymphocytes. In the adults, the LPS-induced immunosuppression is most pronounced in males - they have a decrease in the production of all the cytokines studied and a decrease in the number of cytotoxic and regulatory T-lymphocytes and B-cells. Conclusion. Thus, in each of the studied age periods - newborn, prepubertal and adult, the sexual differences in the immune system reactions are expressed differently and, apparently, these differences are determined by the content of sex steroid hormones, the concentration of which varies with age.

Effect of moderate physical exercise on the immune system modulation in patients with breast cancer during preoperative chemotherapy: The NEO-RUNNER study.

2021 ◽  
Vol 39 (15_suppl) ◽  
pp. 581-581
Author(s):  
Ornella Garrone ◽  
Andrea Abbona ◽  
Antonella Falletta ◽  
Matteo Paccagnella ◽  
Nicoletta Croce ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Immune System ◽  
Principal Component ◽  
Tnf Α ◽  
Negative Effect ◽  
Potential Negative Effect ◽  
Ifn Γ ◽  
The Difference ◽  
Immune System Modulation ◽  
Inflammatory Effect

581 Background: The link between physical activity (PA) and the immune system (IS) is known. However, it is not yet fully understood the immune mechanisms activated by PA. We investigated the immune effect of moderate PA (MPA), nordic or fit walking, during neoadjuvant chemotherapy (NACT) in patients (pts) with breast cancer. Methods: Pts received sequential epirubicin and cyclophosphamide for 4 cycles followed by paclitaxel for 12 weeks. Blood samples from pts underwent MPA (TR) were collected before starting chemotherapy (CT) at baseline (T0), at day 1 of week 6 of paclitaxel (before starting MPA) (T1), before surgery (S) (T2) and after S (T3). Samples were also collected in a group of pts who declined MPA (UN) at the same time points and in 15 healthy volunteers (HV). MPA consisted of 3 workouts per week, 1 hour each, in the 9 weeks before S. At each time point the level of 17 cytokines (IL-2, IL-4, IL-5, IL-6, IL-8, IL-10, IL-12, IL-13, IL-15, CCL-2, CCL-4, CXCL-10, CCL-22, IFN-γ, TGF-β, TNF-α, VEGF) was measured. The difference among the median value of cytokines was analyzed using non parametric Mann Whitney U test. Principal component analysis (PCA) was computed to compare the best discriminating cytokine, identified by ROC analysis, of pts at T1, T2, T3 and in HV. Each patient was distributed in the PCA. Pts having similar cytokine values were plotted in the near position. Normalized values of 8 cytokines (IL-2, IL-4, IL-5, IL-6, IL-13, IL-15, CCL-2, VEGF) were used in PCA. Results: Data from 27 pts are available: 10 TR and 17 UN. A significant increase of IFN-γ, IL-5, IL-8, CCL-2 and CXCL-10 between T0 and T1 (P = 0.004, P = 0.013, P = 0.032, P = 0.046, P = 0.046, respectively) was found in the whole population. CXCL-10 significantly increased also between T1 and T2 in UN pts (P = 0.033). TR pts showed a significant lower level of IL-6, IL-13, CCL-2 at T2 (P = 0.012, P = 0.038, P = 0.023) and higher IL-15 level at T3 (P = 0.047) compared to UN pts. Moreover, a significant decrease of IL-5 was observed between T2 and T3 (P = 0.031). PCA showed that TR and UN pts were mixed at T1. HV were clustered all together and distinct from pts. At T2 TR pts moved toward HV and mixed with them while UN remained separated. TR pts tended to separate from HV at T3, while UN pts still remained distinct. Conclusions: NACT upregulated median values of IFN-γ, IL-5, IL-8, CCL-2 and CXCL-10; CXCL-10 value continues to increase during CT only in UN pts supporting the inflammatory effect of CT. On the contrary, during MPA the level of IL-6, IL-13, CCL-2 decreases in TR compared to UN pts. All together these data suggest that MPA damps the inflammatory response to NACT. Our results show that the majority of TR pts reach an immune profile similar to that of HV in PCA. However, at T3 the effect of MPA is dampened, suggesting a potential negative effect of S.

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