scholarly journals Donor-Specific Regulatory T Cells Acquired from Tolerant Mice Bearing Cardiac Allograft Promote Mixed Chimerism and Prolong Intestinal Allograft Survival

2016 ◽  
Vol 7 ◽  
Author(s):  
Xiao-Fei Shen ◽  
Jin-Peng Jiang ◽  
Jian-Jun Yang ◽  
Wei-Zhong Wang ◽  
Wen-Xian Guan ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Cardiac Allograft ◽  
Mixed Chimerism ◽  
Allograft Survival

scholarly journals Expression Profiling of Murine Double-Negative Regulatory T Cells Suggest Mechanisms for Prolonged Cardiac Allograft Survival

2005 ◽  
Vol 174 (8) ◽  
pp. 4535-4544 ◽  
Author(s):  
Boris P.-L. Lee ◽  
Elaine Mansfield ◽  
Szu-Chuan Hsieh ◽  
Tina Hernandez-Boussard ◽  
Wenhao Chen ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Expression Profiling ◽  
Cardiac Allograft ◽  
Double Negative ◽  
Allograft Survival

scholarly journals IL-33 Expands Suppressive CD11b+Gr-1intand Regulatory T Cells, including ST2L+Foxp3+Cells, and Mediates Regulatory T Cell-Dependent Promotion of Cardiac Allograft Survival

2011 ◽  
Vol 187 (9) ◽  
pp. 4598-4610 ◽  
Author(s):  
Hēth R. Turnquist ◽  
Zhenlin Zhao ◽  
Brian R. Rosborough ◽  
Quan Liu ◽  
Antonino Castellaneta ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Regulatory T Cells ◽  
Regulatory T Cell ◽  
Cardiac Allograft ◽  
Allograft Survival

scholarly journals The Mandible Ameliorates Facial Allograft Rejection and Is Associated with the Development of Regulatory T Cells and Mixed Chimerism

2021 ◽  
Vol 22 (20) ◽  
pp. 11104
Author(s):  
Dante De Paz ◽  
Ana Elena Aviña ◽  
Esteban Cardona ◽  
Chin-Ming Lee ◽  
Chia-Hsien Lin ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Lymph Nodes ◽  
Oral Mucosa ◽  
Immunosuppressive Drugs ◽  
Mixed Chimerism ◽  
Allograft Survival ◽  
T Helper 1 ◽  
Significant Prolongation ◽  
Anti Inflammatory

Vascularized composite allografts contain various tissue components and possess relative antigenicity, eliciting different degrees of alloimmune responses. To investigate the strategies for achieving facial allograft tolerance, we established a mouse hemiface transplant model, including the skin, muscle, mandible, mucosa, and vessels. However, the immunomodulatory effects of the mandible on facial allografts remain unclear. To understand the effects of the mandible on facial allograft survival, we compared the diversities of different facial allograft-elicited alloimmunity between a facial osteomyocutaneous allograft (OMC), including skin, muscle, oral mucosa, and vessels, and especially the mandible, and a myocutaneous allograft (MC) including the skin, muscle, oral mucosa, and vessels, but not the mandible. The different facial allografts of a BALB/c donor were transplanted into a heterotopic neck defect on fully major histocompatibility complex-mismatched C57BL/6 mice. The allogeneic OMC (Allo-OMC) group exhibited significant prolongation of facial allograft survival compared to the allogeneic MC group, both in the presence and absence of FK506 immunosuppressive drugs. With the use of FK506 monotherapy (2 mg/kg) for 21 days, the allo-OMC group, including the mandible, showed prolongation of facial allograft survival of up to 65 days, whereas the myocutaneous allograft, without the mandible, only survived for 34 days. The Allo-OMC group also displayed decreased lymphocyte infiltration into the facial allograft. Both groups showed similar percentages of B cells, T cells, natural killer cells, macrophages, and dendritic cells in the blood, spleen, and lymph nodes. However, a decrease in pro-inflammatory T helper 1 cells and an increase in anti-inflammatory regulatory T cells were observed in the blood and lymph nodes of the Allo-OMC group. Significantly increased percentages of donor immune cells were also observed in three lymphoid organs of the Allo-OMC group, suggesting mixed chimerism induction. These results indicated that the mandible has the potential to induce anti-inflammatory effects and mixed chimerism for prolonging facial allograft survival. The immunomodulatory understanding of the mandible could contribute to reducing the use of immunosuppressive regimens in clinical face allotransplantation including the mandible.

PROLONGATION OF CARDIAC ALLOGRAFT SURVIVAL BY EX VIVO EXPANSION OF SELECTED FOXP3-TRANSDUCED CD4 REGULATORY T CELLS

2008 ◽  
Vol 86 (Supplement) ◽  
pp. 485
Author(s):  
M Hu ◽  
Y M. Wang ◽  
G Y. Zhang ◽  
D Watson ◽  
J Fletcher ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Ex Vivo ◽  
Ex Vivo Expansion ◽  
Cardiac Allograft ◽  
Allograft Survival

scholarly journals ‘Default’ generated neonatal regulatory T cells are hypomethylated at conserved non-coding sequence 2 and promote long-term cardiac allograft survival

Immunology ◽  
2014 ◽  
Vol 143 (4) ◽  
pp. 618-630 ◽  
Author(s):  
Chao Cheng ◽  
Sihua Wang ◽  
Ping Ye ◽  
Xiaofan Huang ◽  
Zheng Liu ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Cardiac Allograft ◽  
Allograft Survival ◽  
Coding Sequence

scholarly journals MiR-146a regulates regulatory T cells to suppress heart transplant rejection in mice

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Jian Lu ◽  
Weiwei Wang ◽  
Peiyuan Li ◽  
Xiaodong Wang ◽  
Chao Gao ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Heart Transplant ◽  
Transplant Rejection ◽  
Mouse Heart ◽  
Allograft Survival ◽  
Treg Function ◽  
Ifn Γ ◽  
Heart Transplant Rejection

AbstractRegulatory T cells (Tregs), which characteristically express forkhead box protein 3 (Foxp3), are essential for the induction of immune tolerance. Here, we investigated microRNA-146a (miR-146a), a miRNA that is widely expressed in Tregs and closely related to their homeostasis and function, with the aim of enhancing the function of Tregs by regulating miR-146a and then suppressing transplant rejection. The effect of the absence of miR-146a on Treg function in the presence or absence of rapamycin was detected in both a mouse heart transplantation model and cell co-cultures in vitro. The absence of miR-146a exerted a mild tissue-protective effect by transiently prolonging allograft survival and reducing the infiltration of CD4+ and CD8+ T cells into the allografts. Meanwhile, the absence of miR-146a increased Treg expansion but impaired the ability of Tregs to restrict T helper cell type 1 (Th1) responses. A miR-146a deficiency combined with interferon (IFN)-γ blockade repaired the impaired Treg function, further prolonged allograft survival, and alleviated rejection. Importantly, miR-146a regulated Tregs mainly through the IFN-γ/signal transducer and activator of transcription (STAT) 1 pathway, which is implicated in Treg function to inhibit Th1 responses. Our data suggest miR-146a controls a specific aspect of Treg function, and modulation of miR-146a may enhance Treg efficacy in alleviating heart transplant rejection in mice.

P761The effect of extracorporeal photopheresis on cardiac allograft rejection and on lymphocyte subclasses

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
T Teszak ◽  
A Assabiny ◽  
A Kiraly ◽  
Z Tarjanyi ◽  
N Parazs ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
B Lymphocytes ◽  
Heart Transplant ◽  
Allograft Rejection ◽  
Cytotoxic T Cells ◽  
Cardiac Allograft ◽  
Extracorporeal Photopheresis ◽  
Cardiac Allograft Rejection ◽  
Cellular Rejection

Abstract Background Cardiac allograft rejection is known to have a profound impact on graft survival and mortality after heart transplant. Previous data on the efficacy of extracorporeal photopheresis (ECP) in the management of cardiac allograft rejection is encouraging. Though, clear evidence on the exact indication and data regarding its effect on distinct lymphocyte subtypes are still lacking. Based on their cytokine production, both helper and cytotoxic T cells can differentiate into either regulatory cells participating in the suppression of rejection or into effector cells responsible for its maintenance. Regulatory T cells are essential for the termination of rejection, while B lymphocytes and natural killer (NK) cells contribute to it. Purpose We aimed to investigate the anti-rejection efficacy and the impact of ECP on peripheral blood lymphocyte subclasses in adult heart transplant recipients. Methods In a retrospective analysis of 12 consecutive patients treated with ECP for cardiac allograft rejection between 2013 and 2019, we examined the grade of rejection in endomyocardial biopsies (EMB) based on the International Society for Heart and Lung Transplantation classification. We analysed the absolute counts and the percentages of helper, cytotoxic and regulatory T cells, B lymphocytes and NK cells with fluorescence activated cell sorting. Measurements were performed both before and after the ECP treatment period. Data values were given as either mean±standard deviation or median [min–max]. Results The patients underwent 26 [2–39] ECP treatments in addition to standard immunosuppressant therapy. Whereas grade 2R cellular rejection was detected in 83% of the cases prior to initiating ECP, none of the examined EMB specimen revealed rejection greater than grade 1R cellular rejection post ECP therapy. The average grade of cellular rejection improved significantly (1.25±0.45 vs. 0.50±0.53; p=0.022). The absolute count and the percentage of helper T cells increased significantly post ECP therapy (0.34 G/l±0.26 G/l vs. 0.51 G/l±0.39 G/l; p=0.018 and 3.43%±2.24% vs. 5.98%±3.64%; p=0.017, respectively). There was also a significant rise in the percentage of cytotoxic T cells (2.33%±1.46% vs. 4.16±2.98%; p=0.027). We noticed an almost significant twofold increase in the percentage of regulatory T cells on completion of the ECP therapy (0.20%±0.22% vs. 0.37%±0.20%; p=0.060). Neither B lymphocyte nor NK cell counts revealed any significant changes. Conclusion ECP was effective in reducing the severity of cardiac allograft rejection episodes. The significant decrease in rejection rates might be indicative of the predominance of anti-inflammatory helper and cytotoxic T cell subpopulations and the increase of regulatory T cell count post ECP therapy. However, discussion of the results are limited by small sample size and the effect of medical therapy on the lymphocytes.

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