scholarly journals Polyclonal CD4+Foxp3+ Treg cells induce TGFβ-dependent tolerogenic dendritic cells that suppress the murine lupus-like syndrome

2012 ◽  
Vol 4 (6) ◽  
pp. 409-419 ◽  
Author(s):  
Qin Lan ◽  
Xiaohui Zhou ◽  
Huimin Fan ◽  
Maogen Chen ◽  
Julie Wang ◽  
...  
2016 ◽  
Vol 118 ◽  
pp. 110
Author(s):  
Akemi Ushijima ◽  
Tomoko Shima ◽  
Kumiko Inada ◽  
Akitoshi Nakashima ◽  
Osamu Yoshino ◽  
...  

2017 ◽  
Vol 32 (0) ◽  
pp. 13-20
Author(s):  
Akemi Ushijima ◽  
Tomoko Shima ◽  
Kumiko Inada ◽  
Akitoshi Nakashima ◽  
Osamu Yoshino ◽  
...  

2014 ◽  
Vol 21 (16) ◽  
pp. 1898-1909 ◽  
Author(s):  
Enrique Vacas-Cordoba ◽  
Hugo Bastida ◽  
Marjorie Pion ◽  
Aurelien Hameau ◽  
Maksim Ionov ◽  
...  

Cytotherapy ◽  
2021 ◽  
Vol 23 (3) ◽  
pp. 242-255
Author(s):  
Kayleigh M. van Megen ◽  
Zhuo Chen ◽  
Antoinette M. Joosten ◽  
Sandra Laban ◽  
Jaap-Jan Zwaginga ◽  
...  

2021 ◽  
Vol 70 ◽  
pp. 33-39
Author(s):  
Andreia Barroso ◽  
João V Mahler ◽  
Pedro H Fonseca-Castro ◽  
Francisco J Quintana

2019 ◽  
Vol 28 (3) ◽  
pp. 265-272
Author(s):  
Sang Youn Jung ◽  
Kil-Sang Cho ◽  
Doo-Rye Jang ◽  
Jun-Ho Lee ◽  
So-Yeon Choi ◽  
...  

2011 ◽  
Vol 9 (1) ◽  
pp. 89 ◽  
Author(s):  
M Naranjo-Gómez ◽  
D Raïch-Regué ◽  
C Oñate ◽  
L Grau-López ◽  
C Ramo-Tello ◽  
...  

2014 ◽  
Vol 2014 ◽  
pp. 1-12 ◽  
Author(s):  
Jie Yang ◽  
Yiming Yang ◽  
Huahua Fan ◽  
Hejian Zou

TGF-β-induced regulatory T cells (iTregs) retain Foxp3 expression and immune-suppressive activity in collagen-induced arthritis (CIA). However, the mechanisms whereby transferred iTregs suppress immune responses, particularly the interplay between iTregs and dendritic cells (DCs)in vivo, remain incompletely understood. In this study, we found that after treatment with iTregs, splenic CD11c+DCs, termed “DCiTreg,” expressed tolerogenic phenotypes, secreted high levels of IL-10, TGF-β, and IDO, and showed potent immunosuppressive activityin vitro. After reinfusion with DCiTreg, marked antiarthritic activity improved clinical scores and histological end-points were observed. The serological levels of inflammatory cytokines and anti-CII antibodies were low and TGF-βproduction was high in the DCiTreg-treated group. DCiTregalso induced new iTregsin vivo. Moreover, the inhibitory activity of DCiTregon CIA was lost following pretreatment with the inhibitor of indoleamine 2,3-dioxygenase (IDO). Collectively, these findings suggest that transferred iTregs could induce tolerogenic characteristics in splenic DCs and these cells could effectively dampen CIA in an IDO-dependent manner. Thus, the potential therapeutic effects of iTregs in CIA are likely maintained through the generation of tolerogenic DCsin vivo.


2013 ◽  
Vol 191 (5) ◽  
pp. 2247-2257 ◽  
Author(s):  
Takuya Matsumoto ◽  
Hitoshi Hasegawa ◽  
Sachiko Onishi ◽  
Jun Ishizaki ◽  
Koichiro Suemori ◽  
...  

2010 ◽  
Vol 78 (11) ◽  
pp. 4763-4772 ◽  
Author(s):  
Raquel M. Gonçalves ◽  
Karina C. Salmazi ◽  
Bianca A. N. Santos ◽  
Melissa S. Bastos ◽  
Sandra C. Rocha ◽  
...  

ABSTRACT Clearing blood-stage malaria parasites without inducing major host pathology requires a finely tuned balance between pro- and anti-inflammatory responses. The interplay between regulatory T (Treg) cells and dendritic cells (DCs) is one of the key determinants of this balance. Although experimental models have revealed various patterns of Treg cell expansion, DC maturation, and cytokine production according to the infecting malaria parasite species, no studies have compared all of these parameters in human infections with Plasmodium falciparum and P. vivax in the same setting of endemicity. Here we show that during uncomplicated acute malaria, both species induced a significant expansion of CD4+ CD25+ Foxp3+ Treg cells expressing the key immunomodulatory molecule CTLA-4 and a significant increase in the proportion of DCs that were plasmacytoid (CD123+), with a decrease in the myeloid/plasmacytoid DC ratio. These changes were proportional to parasite loads but correlated neither with the intensity of clinical symptoms nor with circulating cytokine levels. One-third of P. vivax-infected patients, but no P. falciparum-infected subjects, showed impaired maturation of circulating DCs, with low surface expression of CD86. Although vivax malaria patients overall had a less inflammatory cytokine response, with a higher interleukin-10 (IL-10)/tumor necrosis factor alpha (TNF-α) ratio, this finding did not translate to milder clinical manifestations than those of falciparum malaria patients. We discuss the potential implications of these findings for species-specific pathogenesis and long-lasting protective immunity to malaria.


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