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M. Di Ianni B. Del Papa D. Cecchini E. Bonifacio L. Moretti T. Zei R. Iacucci Ostini F. Falzetti L. Fontana G. Tagliapietra C. Maldini M. F. Martelli A. Tabilio 《Clinical and experimental immunology》2009,156(2):246-253
Although CD4+/CD25+ T regulatory cells (Tregs) are a potentially powerful tool in bone marrow transplantation, a prerequisite for clinical use is a cell‐separation strategy complying with good manufacturing practice guidelines. We isolated Tregs from standard leukapheresis products using double‐negative selection (anti‐CD8 and anti‐CD19 monoclonal antibodies) followed by positive selection (anti‐CD25 monoclonal antibody). The final cell fraction (CD4+/CD25+) showed a mean purity of 93·6% ± 1·1. Recovery efficiency was 81·52% ± 7·4. The CD4+/CD25+bright cells were 28·4% ± 6·8. The CD4+/CD25+ fraction contained a mean of 51·9% ± 15·1 FoxP3 cells and a mean of 18·9% ± 11·5 CD127 cells. Increased FoxP3 and depleted CD127 mRNAs in CD4+CD25+FoxP3+ cells were in line with flow cytometric results. In Vβ spectratyping the complexity scores of CD4+/CD25+ cells and CD4+/CD25‐ cells were not significantly different, indicating that Tregs had a broad T cell receptor repertoire. The inhibition assay showed that CD4+/CD25+ cells inhibited CD4+/CD25‐ cells in a dose‐dependent manner (mean inhibition percentages: 72·4 ± 8·9 [ratio of T responder (Tresp) to Tregs, 1:2]; 60·8% ± 20·5 (ratio of Tresp to Tregs, 1:1); 25·6 ± 19·6 (ratio of Tresp to Tregs, 1:0·1)). Our study shows that negative/positive Treg selection, performed using the CliniMACS device and reagents, enriches significantly CD4+CD25+FoxP3+ cells endowed with immunosuppressive capacities. The CD4+CD25+FoxP3+ population is a source of natural Treg cells that are depleted of CD8+ and CD4+/CD25‐ reacting clones which are potentially responsible for triggering graft‐versus‐host disease (GvHD). Cells isolated by means of this approach might be used in allogeneic haematopoietic cell transplantation to facilitate engraftment and reduce the incidence and severity of GvHD without abrogating the potential graft‐versus‐tumour effect. 相似文献
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A. U. Engela M. J. Hoogduijn K. Boer N. H. R. Litjens M. G. H. Betjes W. Weimar C. C. Baan 《Clinical and experimental immunology》2013,173(2):343-354
Due to their immunomodulatory properties, mesenchymal stem cells (MSC) are interesting candidates for cellular therapy for autoimmune disorders, graft‐versus‐host disease and allograft rejection. MSC inhibit the proliferation of effector T cells and induce T cells with a regulatory phenotype. So far it is unknown whether human MSC‐induced CD4+CD25+CD127–forkhead box P3 (FoxP3)+ T cells are functional and whether they originate from effector T cells or represent expanded natural regulatory T cells (nTreg). Perirenal adipose‐tissue derived MSC (ASC) obtained from kidney donors induced a 2·1‐fold increase in the percentage of CD25+CD127–FoxP3+ cells within the CD4+ T cell population from allostimulated CD25–/dim cells. Interleukin (IL)‐2 receptor blocking prevented this induction. The ASC‐induced T cells (iTreg) inhibited effector cell proliferation as effectively as nTreg. The vast majority of cells within the iTreg fraction had a methylated FOXP3 gene Treg‐specific demethylated region (TSDR) indicating that they were not of nTreg origin. In conclusion, ASC induce Treg from effector T cells. These iTreg have immunosuppressive capacities comparable to those of nTreg. Their induction is IL‐2 pathway‐dependent. The dual effect of MSC of inhibiting immune cell proliferation while generating de‐novo immunosuppressive cells emphasizes their potential as cellular immunotherapeutic agent. 相似文献
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《Human immunology》2016,77(1):20-28
CD8-positive γδ T lymphocytes (GDCD8+) are specifically increased in peripheral blood of Behçet’s disease (BD) patients. GDCD8+ have shown a T regulatory (Treg) function in autoimmune experimental models, human tumor infiltrates and intestinal intraepithelial lymphocytes from celiac patients. The aim of this study was to evaluate the Treg function of GDCD8+ and GDCD8−, freshly isolated from peripheral blood, in comparison to CD4+CD25high naturally occurring Treg cells (nTreg) in BD and healthy controls (HC).We tested their suppressive activity on CD4+CD25− T effector cells (Teff) proliferation by a CFSE dilution protocol, after suboptimal activation with anti-CD3, in the absence or presence of IL-2. Furthermore, secreted cytokines and suppressive latency associated peptide (LAP)-TGFβ surface upregulation were determined after GD activation.We found that Vδ1 chains contribution to GDCD8+ was higher in BD than in HC, but neither GDCD8+ nor GDCD8−; (i) suppressed Teff proliferation, (ii) expressed LAP-TGFβ (iii) nor secreted IL-10, in either group. Moreover, GD presented a proinflammatory cytokine profile, mainly producing IFNγ and TNFα, in contrast to nTregs.In conclusion, peripheral GD could contribute more to the dysregulation of TH1 type of cytokines than to exerting a Treg function in BD. 相似文献
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Decreased FOXP3 protein expression in patients with asthma 总被引:1,自引:0,他引:1
S. Provoost T. Maes Y. M. van Durme P. Gevaert C. Bachert C. B. Schmidt-Weber G. G. Brusselle G. F. Joos K. G. Tournoy 《Allergy》2009,64(10):1539-1546
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T. Bollinger A. Bollinger L. Skrum S. Dimitrov T. Lange W. Solbach 《Clinical and experimental immunology》2009,155(2):231-238
A number of immunological functions are dependent on circadian rhythms and regular sleep. This has impact on the type and magnitude of immune responses following antigenic challenge, for example in vaccination. Little is known about the underlying mechanisms. One possibility may be the circadian and sleep‐dependent modulation of CD4+CD25‐ T cell responses by CD4+CD25+ natural regulatory T cells (nTreg). In a variety of studies, nTreg have been shown to regulate T cell responses negatively. Thus, we investigated the influence of sleep and circadian rhythm on the number and function of nTreg as well as on the function of CD4+CD25‐ T cells. Seven healthy young men were examined under defined conditions on two occasions, i.e. during sleep and sleep deprivation. Venous blood was drawn periodically; numbers of nTreg, suppressive activity of nTreg, interleukin‐2 production and proliferation of CD4+CD25‐ T cells were explored in vitro. nTreg counts revealed a significant circadian rhythm with highest levels during the night (mean 95 nTreg/µl) and lowest levels during the day (mean 55 nTreg/µl). During normal sleep, the suppressive activity of nTreg was highest at 02.00 h and somewhat lower at 15.00 h. Surprisingly, almost no suppressive activity was present at 07.00 h. Deprivation of sleep abrogated this rhythm. CD4+CD25– T cell proliferation was dampened significantly by sleep deprivation. This is the first study in human cells to show that nTreg number and function follow a rhythm across the 24‐h period. Furthermore, sleep deprivation severely disturbs the functional rhythm of nTreg and CD4+CD25– T cells. 相似文献
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Decreased frequencies and impaired functions of the CD31+ subpopulation in Treg cells associated with decreased FoxP3 expression and enhanced Treg cell defects in patients with coronary heart disease
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L. Huang Y. Zheng X. Yuan Y. Ma G. Xie W. Wang H. Chen L. Shen 《Clinical and experimental immunology》2017,187(3):441-454
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Two separate effects contribute to regulatory T cell defect in systemic lupus erythematosus patients and their unaffected relatives
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N. Costa O. Marques S. I. Godinho C. Carvalho B. Leal A. M. Figueiredo C. Vasconcelos A. Marinho M. F. Moraes‐Fontes A. Gomes da Costa C. Ponte R. Campanilho‐Marques T. Cóias A. R. Martins J. F. Viana M. Lima B. Martins C. Fesel 《Clinical and experimental immunology》2017,189(3):318-330
Forkhead box P3 (FoxP3)+ regulatory T cells (Tregs) are functionally deficient in systemic lupus erythematosus (SLE), characterized by reduced surface CD25 [the interleukin (IL)‐2 receptor alpha chain]. Low‐dose IL‐2 therapy is a promising current approach to correct this defect. To elucidate the origins of the SLE Treg phenotype, we studied its role through developmentally defined regulatory T cell (Treg) subsets in 45 SLE patients, 103 SLE‐unaffected first‐degree relatives and 61 unrelated healthy control subjects, and genetic association with the CD25‐encoding IL2RA locus. We identified two separate, uncorrelated effects contributing to Treg CD25. (1) SLE patients and unaffected relatives remarkably shared CD25 reduction versus controls, particularly in the developmentally earliest CD4+FoxP3+CD45RO–CD31+ recent thymic emigrant Tregs. This first component effect influenced the proportions of circulating CD4+FoxP3highCD45RO+ activated Tregs. (2) In contrast, patients and unaffected relatives differed sharply in their activated Treg CD25 state: while relatives as control subjects up‐regulated CD25 strongly in these cells during differentiation from naive Tregs, SLE patients specifically failed to do so. This CD25 up‐regulation depended upon IL2RA genetic variation and was related functionally to the proliferation of activated Tregs, but not to their circulating numbers. Both effects were found related to T cell IL‐2 production. Our results point to (1) a heritable, intrathymic mechanism responsible for reduced CD25 on early Tregs and decreased activation capacity in an extended risk population, which can be compensated by (2) functionally independent CD25 up‐regulation upon peripheral Treg activation that is selectively deficient in patients. We expect that Treg‐directed therapies can be monitored more effectively when taking this distinction into account. 相似文献
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M.‐T. Dieterlen H. B. Bittner A. Pierzchalski S. Dhein F. W. Mohr M. J. Barten 《Clinical and experimental immunology》2014,176(1):120-128
Extracorporeal photopheresis (ECP) has been used as a prophylactic and therapeutic option to avoid and treat rejection after heart transplantation (HTx). Tolerance‐inducing effects of ECP such as up‐regulation of regulatory T cells (Tregs) are known, but specific effects of ECP on regulatory T cell (Treg) subsets and dendritic cells (DCs) are lacking. We analysed different subsets of Tregs and DCs as well as the immune balance status during ECP treatment after HTx. Blood samples were collected from HTx patients treated with ECP for prophylaxis (n = 9) or from patients with histologically proven acute cellular rejection (ACR) of grade ≥ 1B (n = 9), as well as from control HTx patients without ECP (HTxC; n = 7). Subsets of Tregs and DCs as well as different cytokine levels were analysed. Almost 80% of the HTx patients showed an effect to ECP treatment with an increase of Tregs and plasmacytoid DCs (pDCs). The percentage of pDCs before ECP treatment was significantly higher in patients with no ECP effect (26·3% ± 5·6%) compared to patients who showed an effect to ECP (9·8% ± 10·2%; P = 0·011). Analysis of functional subsets of CD4+CD25highCD127low Tregs showed that CD62L‐, CD120b‐ and CD147‐positive Tregs did not differ between the groups. CD39‐positive Tregs increased during ECP treatment compared to HTxC. ECP‐treated patients showed higher levels for T helper type 1 (Th1), Th2 and Th17 cytokines. Cytokine levels were higher in HTx patients with rejection before ECP treatment compared to patients with prophylactic ECP treatment. We recommend a monitoring strategy that includes the quantification and analysis of Tregs, pDCs and the immune balance status before and up to 12 months after starting ECP. 相似文献
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J. Saison T. Ferry J. Demaret D Maucort Boulch F. Venet T. Perpoint F. Ader V. Icard C. Chidiac G. Monneret Lyon HIV Cohort Study 《Clinical and experimental immunology》2014,176(3):401-409
The mechanisms sustaining the absence of complete immune recovery in HIV‐infected patients upon long‐term effective highly active anti‐retroviral therapy (HAART) remain elusive. Immune activation, regulatory T cells (Tregs) or very low‐level viraemia (VLLV) have been alternatively suspected, but rarely investigated simultaneously. We performed a cross‐sectional study in HIV‐infected aviraemic subjects (mean duration of HAART: 12 years) to concomitantly assess parameters associated independently with inadequate immunological response. Patients were classified as complete immunological responders (cIR, n = 48) and inadequate immunological responders (iIR, n = 39), depending on the CD4+ T cell count (> or < 500/mm3). Clinical and virological data (including very low‐level viraemia) were collected. In parallel, immunophenotyping of CD4+ lymphocytes, including Treg subsets, and CD8+ T cells was performed. Percentages of activated CD4+ T cells, Tregs, effector Tregs and terminal effector Tregs were found to be significantly elevated in iIR. Neither the percentage of activated CD8+ T cells nor VLLV were found to be associated with iIR. In the multivariate analysis, nadir of CD4+ T cell count and percentage of Tregs were the only two parameters associated independently with iIR [odds ratio (OR) = 2·339, P = 0·001, and OR = 0·803, P = 0·041]. We present here the largest study investigating simultaneously the immune response to long‐term HAART, activation of CD4+ and CD8+ T cells, Treg percentages and very low‐level viraemia. Causative interactions between Tregs and CD4+ T cells should now be explored prospectively in a large patients cohort. 相似文献
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CD4+ T cell anergy reflects the inability of CD4+ T cells to respond functionally to antigenic stimulation through proliferation or IL‐2 secretion. Histone deacetylase (HDAC) inhibitors have been shown to induce anergy in antigen‐activated CD4+ T cells. However, questions remain if HDAC inhibitors mediate anergy through direct action upon activated CD4+ T cells or through the generation and/or enhancement of regulatory T (Treg) cells. To assess if HDAC inhibitor n‐butyrate induces anergy independent of the generation or expansion of FoxP3+ Treg cells in vitro, we examine n‐butyrate‐treated murine CD4+ T cells for anergy induction and FoxP3+ Treg activity. Whereas n‐butyrate decreases CD4+ T cell proliferation and IL‐2 secretion, n‐butyrate did not augment FoxP3 protein production or confer a suppressive phenotype upon CD4+ T cells. Collectively, these data suggest that HDAC inhibitors can facilitate CD4+ T cell functional unresponsiveness directly and independently of Treg cell involvement. 相似文献
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Significant augmentation of regulatory T cell numbers occurs during the early neonatal period
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Regulatory T cells (Tregs) control immune responses by suppressing various inflammatory cells. Tregs in newborn babies may play an important role in preventing excessive immune responses during their environmental change. We examined the number and phenotype of Tregs during the neonatal period in 49 newborn babies. Tregs were characterized by flow cytometry using cord blood (CB) and peripheral blood (PB) from the early (7–8 days after birth) and late (2–4 weeks after birth) neonatal periods. CD4+forkhead box protein 3 (FoxP3+) T cells were classified into resting Tregs (CD45RA+FoxP3low), activated Tregs (CD45RA– FoxP3high) and newly activated T cells (CD45RA– FoxP3low). Compared with CB and PB during the late neonatal period, the percentage of Tregs and all Treg subpopulations in the CD4+ lymphocyte population were increased significantly during the early neonatal period. Furthermore, the proportion and absolute number of activated Tregs were increased markedly compared with other Treg subpopulations, such as resting Tregs and newly activated T cells (non‐Tregs), in the early neonatal period. Increased Tregs concomitantly expressed the suppressive molecule cytotoxic T lymphocyte antigen‐4 (CTLA‐4). The up‐regulated expression of chemokine receptor 4 (CCR4) and down‐regulated expression of CCR7 were also observed in expanded Tregs. When cord blood cells were cultured in vitro with CD3 monoclonal antibodies (mAb) for 5 days, CD4+CD45RA–FoxP3high cells were increased significantly during the culture. Thus, the presence of increased activated Tregs in early neonates may play an important role in immunological regulation by suppressing excessive T cell activation caused by the immediate exposure to ubiquitous antigens after birth. 相似文献
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S. M. Toor A. S. Syed Khaja I. Alkurd E. Elkord 《Clinical and experimental immunology》2018,191(2):189-197
Programmed death‐1 (PD‐1) and interactions with PD‐ligand 1 (PD‐L1) play critical roles in the tumour evasion of immune responses through different mechanisms, including inhibition of effector T cell proliferation, reducing cytotoxic activity, induction of apoptosis in tumour‐infiltrating T cells and regulatory T cell (Treg) expansion. Effective blockade of immune checkpoints can therefore potentially eliminate these detrimental effects. The aim of this study was to investigate the effect of anti‐PD‐1 antibody, pembrolizumab, on various Treg subpopulations. Peripheral blood mononuclear cells (PBMC) from healthy donors (HD) and primary breast cancer patients (PBC) were treated in vitro with pembrolizumab, which effectively reduced PD‐1 expression in both cohorts. We found that PD‐1 was expressed mainly on CD4+CD25+ T cells and pembrolizumab had a greater effect on PD‐1 expression in CD4+CD25? T cells, compared to CD4+CD25+ cells. In addition, pembrolizumab did not affect the expression levels of Treg‐related markers, including cytotoxic T lymphocyte antigen‐4 (CTLA‐4), CD15s, latency‐associated peptide (LAP) and Ki‐67. Moreover, we report that CD15s is expressed mainly on forkhead box P3 (FoxP3)?Helios+ Treg in HD, but it is expressed on FoxP3+Helios? Treg subset in addition to FoxP3?Helios+ Treg in PBC. Pembrolizumab did not affect the levels of FoxP3+/?Helios+/? Treg subsets in both cohorts. Taken together, our study suggests that pembrolizumab does not affect Treg or change their phenotype or function but rather blocks signalling via the PD‐1/PD‐L1 axis in activated T cells. 相似文献
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N. Yokobori C. Sabio y García R. Musella J. Castagnino M. C. Sasiain S. de la Barrera 《Clinical and experimental immunology》2014,175(2):235-245
Tuberculous pleural effusion is characterized by a T helper type 1 (Th1) profile, but an excessive Th1 response may also cause tissue damage that might be controlled by regulatory mechanisms. In the current study we investigated the role of regulatory T cells (Treg) in the modulation of Th1 responses in patients with tuberculous (TB) pleurisy. Using flow cytometry we evaluated the proportion of Treg (CD4+CD25highforkhead box protein 3+), interferon (IFN)‐γ and interleukin (IL)‐10 expression and CD107 degranulation in peripheral blood (PB) and pleural fluid (PF) from patients with TB pleurisy. We demonstrated that the proportion of CD4+CD25+, CD4+CD25highFoxP3+ and CD8+CD25+ cells were increased in PF compared to PB samples. Mycobacterium tuberculosis stimulation increased the proportion of CD4+CD25low/negIL‐10+ in PB and CD4+CD25low/negIFN‐γ+ in PF; meanwhile, CD25high mainly expressed IL‐10 in both compartments. A high proportion of CD4+CD107+ and CD8+CD107+ cells was observed in PF. Treg depletion enhanced the in‐vitro M. tuberculosis‐induced IFN‐γ and CD4+ and CD8+ degranulation responses and decreased CD4+IL‐10+ cells in PF. Our results demonstrated that in TB pleurisy Treg cells effectively inhibit not only IFN‐γ expression but also the ability of CD4+ and CD8+ cells to degranulate in response to M. tuberculosis. 相似文献
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Harnessing the power of regulatory T‐cells to control autoimmune diabetes: overview and perspective
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Type 1 diabetes (T1D) is a T‐cell‐mediated autoimmune disease resulting in islet β‐cell destruction, hypoinsulinaemia and severely altered glucose homeostasis. Although the mechanisms that initiate T1D still remain elusive, a breakdown of immune tolerance between effector T‐cells (Teff) and regulatory T‐cells (Treg) is considered to be the crucial component leading to autoimmunity. As such, strategies have been developed to boost the number and/or function of Treg in the hope of specifically hampering the pathogenic Teff activity. In this review, we will summarize the current understanding of biomarkers and functions of both forkhead box protein 3 (FoxP3)+ Treg and type 1 regulatory T (Tr1) cells in health and in T1D, examine the outcome of experimental therapies in both animal models and humans via manipulation of Treg responses and also provide an outlook on the potential of Treg‐based immunotherapies in the prevention and treatment of this disease. Discussed immunotherapies include adoptive transfer of ex‐vivo expanded FoxP3+ Treg, manipulation of Treg cells via the interleukin (IL)‐2/IL‐2R pathway and induction of Treg by tolerogenic peptides, tolerogenic dendritic cells or altered gut microbiota. 相似文献
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G. Fousteri T. Jofra I. Debernardis S. M. Stanford A. Laurenzi N. Bottini M. Battaglia 《Clinical and experimental immunology》2014,178(1):178-189
Protein tyrosine phosphatases (PTPs) regulate T cell receptor (TCR) signalling and thus have a role in T cell differentiation. Here we tested whether the autoimmune predisposing gene PTPN22 encoding for a PTP that inhibits TCR signalling affects the generation of forkhead box protein 3 (FoxP3)+ T regulatory (Treg) cells and T helper type 1 (Th1) cells. Murine CD4+ T cells isolated from Ptpn22 knock‐out (Ptpn22KO) mice cultured in Treg cell polarizing conditions showed increased sensitivity to TCR activation compared to wild‐type (WT) cells, and subsequently reduced FoxP3 expression at optimal‐to‐high levels of activation. However, at lower levels of TCR activation, Ptpn22KO CD4+ T cells showed enhanced expression of FoxP3. Similar experiments in humans revealed that at optimal levels of TCR activation PTPN22 knock‐down by specific oligonucleotides compromises the differentiation of naive CD4+ T cells into Treg cells. Notably, in vivo Treg cell conversion experiments in mice showed delayed kinetic but overall increased frequency and number of Treg cells in the absence of Ptpn22. In contrast, the in vitro and in vivo generation of Th1 cells was comparable between WT and Ptpn22KO mice, thus suggesting PTPN22 as a FoxP3‐specific regulating factor. Together, these results propose PTPN22 as a key factor in setting the proper threshold for FoxP3+ Treg cell differentiation. 相似文献
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Novel therapeutic compound tuftsin–phosphorylcholine attenuates collagen‐induced arthritis
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T. Bashi O. Shovman M. Fridkin A. Volkov I. Barshack M. Blank Y. Shoenfeld 《Clinical and experimental immunology》2016,184(1):19-28
Treatment with helminthes and helminthes ova improved the clinical symptoms of several autoimmune diseases in patients and in animal models. Phosphorylcholine (PC) proved to be the immunomodulatory molecule. We aimed to decipher the tolerogenic potential of tuftsin–PC (TPC), a novel helminth‐based compound in collagen‐induced arthritis (CIA) a mouse model of rheumatoid arthritis (RA). CIA DBA/1 mice were treated with TPC subcutaneously (5 µg/0.1 ml) or orally (250 µg/0.1 ml), starting prior to disease induction. The control groups were treated with PBS. Collagen antibodies were tested by enzyme‐linked immunosorbent assay (ELISA), cytokine protein levels by ELISA kits and regulatory T (Treg) and regulatory B (Breg) cell phenotypes by fluorescence‐activated cell sorter (FACS). TPC‐treated mice had a significantly lower arthritis score of 1.5 in comparison with control mice 11.8 (P < 0.0001) in both subcutaneous and orally treated groups at day 31. Moreover, histology analysis demonstrated highly inflamed joints in control mice, whereas TPC‐treated mice maintained normal joint structure. Furthermore, TPC decreased the titres of circulating collagen II antibodies in mice sera (P < 0.0001), enhanced expression of IL‐10 (P < 0.0001) and inhibited production of tumour necrosis factor (TNF)‐α, interleukin (IL)?17 and IL‐1β (P < 0.0001). TPC significantly expanded the CD4+CD25+ forkhead box protein 3 (FoxP3+) Treg cells and CD19+IL‐10+CD5highCD1dhighT cell immunoglobulin mucin‐1 (TIM‐1+) Breg cell phenotypes (P < 0.0001) in treated mice. Our data indicate that treatment with TPC attenuates CIA in mice demonstrated by low arthritic score and normal joints histology. TPC treatment reduced proinflammatory cytokines and increased anti‐inflammatory cytokine expression, as well as expansion of Treg and Breg cells. Our results may lead to a new approach for a natural therapy for early rheumatoid arthritis onset. 相似文献