scholarly journals Complement component 3 deficiency prolongs MHC-II disparate skin allograft survival by increasing the CD4+ CD25+ regulatory T cells population

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Quan-you Zheng ◽  
Shen-ju Liang ◽  
Gui-qing Li ◽  
Yan-bo Lv ◽  
You Li ◽  
...  
2014 ◽  
Vol 93 (2) ◽  
pp. 113-119 ◽  
Author(s):  
Mauricio Campos‐Mora ◽  
Rodrigo A Morales ◽  
Francisco Pérez ◽  
Tania Gajardo ◽  
Javier Campos ◽  
...  

2013 ◽  
Vol 191 (8) ◽  
pp. 4447-4455 ◽  
Author(s):  
Melissa Y. Yeung ◽  
Martina M. McGrath ◽  
Masafumi Nakayama ◽  
Tetsunosuke Shimizu ◽  
Olaf Boenisch ◽  
...  

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Jian Lu ◽  
Weiwei Wang ◽  
Peiyuan Li ◽  
Xiaodong Wang ◽  
Chao Gao ◽  
...  

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.


2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Atar Lev ◽  
Amos J. Simon ◽  
Luba Trakhtenbrot ◽  
Itamar Goldstein ◽  
Meital Nagar ◽  
...  

Introduction. Patients with severe combined immunodeficiency (SCID) may present with residual circulating T cells. While all cells are functionally deficient, resulting in high susceptibility to infections, only some of these cells are causing autoimmune symptoms.Methods. Here we compared T-cell functions including the number of circulating CD3+T cells,in vitroresponses to mitogens, T-cell receptor (TCR) repertoire, TCR excision circles (TREC) levels, and regulatory T cells (Tregs) enumeration in several immunodeficinecy subtypes, clinically presenting with nonreactive residual cells (MHC-II deficiency) or reactive cells. The latter includes patients with autoreactive clonal expanded T cell and patients with alloreactive transplacentally maternal T cells.Results. MHC-II deficient patients had slightly reduced T-cell function, normal TRECs, TCR repertoires, and normal Tregs enumeration. In contrast, patients with reactive T cells exhibited poor T-cell differentiation and activity. While the autoreactive cells displayed significantly reduced Tregs numbers, the alloreactive transplacentally acquired maternal lymphocytes had high functional Tregs.Conclusion. SCID patients presenting with circulating T cells show different patterns of T-cell activity and regulatory T cells enumeration that dictates the immunodeficient and autoimmune manifestations. We suggest that a high-tolerance capacity of the alloreactive transplacentally acquired maternal lymphocytes represents a toleration advantage, yet still associated with severe immunodeficiency.


2014 ◽  
Vol 45 (2) ◽  
pp. 452-463 ◽  
Author(s):  
Carolina Moore ◽  
Gabriela Tejon ◽  
Camila Fuentes ◽  
Yessia Hidalgo ◽  
Maria R. Bono ◽  
...  

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