scholarly journals In vitroTNF blockade enhancesex vivoexpansion of regulatory T cells in patients with immune thrombocytopenia

2014 ◽  
Vol 168 (2) ◽  
pp. 274-283 ◽  
Author(s):  
Hui Zhong ◽  
James Bussel ◽  
Karina Yazdanbakhsh
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Immune Thrombocytopenia

Decreased TLR4 expression on monocytes may cause regulatory T cells abnormality in patients with primary immune thrombocytopenia

Autoimmunity ◽  
2017 ◽  
Vol 50 (5) ◽  
pp. 283-292 ◽  
Author(s):  
Yating Hao ◽  
Huiyuan Li ◽  
Yang Li ◽  
Mingen Lyu ◽  
Donglei Zhang ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Immune Thrombocytopenia ◽  
Tlr4 Expression ◽  
Primary Immune Thrombocytopenia

Low dose IL-2 increase regulatory T cells and elevate platelets in a patient with immune thrombocytopenia

2016 ◽  
Vol 94 (3) ◽  
pp. 400-404 ◽  
Author(s):  
Jiakui Zhang ◽  
Yanjie Ruan ◽  
Yuanyuan Shen ◽  
Qianshan Tao ◽  
Huiping Wang ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Immune Thrombocytopenia ◽  
Low Dose

scholarly journals Indirubin Increases CD4+CD25+Foxp3+ Regulatory T Cells to Prevent Immune Thrombocytopenia in Mice

PLoS ONE ◽  
2015 ◽  
Vol 10 (11) ◽  
pp. e0142634 ◽  
Author(s):  
Aijun Zhang ◽  
Bin Ning ◽  
Nianzheng Sun ◽  
Jianlu Wei ◽  
Xiuli Ju
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Immune Thrombocytopenia

Impaired Interaction Between Regulatory T Cells and Dendritic Cells in Immune Thrombocytopenia.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 3511-3511
Author(s):  
Lucia Catani ◽  
Daria Sollazzo ◽  
Antonio Curti ◽  
Sara Trabanelli ◽  
Francesca Palandri ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
T Cells ◽  
Dendritic Cells ◽  
Regulatory T Cells ◽  
Healthy Subjects ◽  
Immune Thrombocytopenia ◽  
Suppressive Activity ◽  
Immune Disorder ◽  
Pathogenetic Role

Abstract Abstract 3511 Poster Board III-448 CD4+CD25+ regulatory T cells (Tregs) are critical in maintaining self-tolerance and preventing organ-specific autoimmune diseases. However, the role of Tregs in the pathogenesis of immune thrombocytopenia (ITP), an immune disorder in which increased platelet clearance is caused by antiplatelet autoantibodies, has not yet been clarified. The purpose of the present study was to investigate whether the interaction between dendritic cells (DCs) and regulatory T cells (Tregs) may play a pathogenetic role in ITP. Forty patients with active disease and 35 healthy subjects were enrolled into the study. We firstly characterized the number (by flow cytometry) and the suppressive activity (by modified allogeneic mixed leukocyte reaction) of Tregs in ITP. We found that the absolute number of Tregs was significantly decreased in ITP patients in comparison to healthy subjects (CD4+CD25highFoxp3+ T cells (5.5±4.3 vs 11.6±6.9 cells/microL; p below 0.01) and CD4+CD25highCD127low-negative T cells (50.9±27.3 vs 80.5±37.7 cells/microL; p below 0.02)). We documented also that in ITP suppressive activity of Tregs was defective as compared to healthy subjects. In parallel experiments we studied the in vitro conversion of CD4+CD25- T cells, either from ITP patients or healthy subjects, into CD4+CD25+Foxp3+ Tregs by co-coltures with mature autologous/allogeneic DCs. The flow cytometry analysis showed that in ITP the low number of circulating Tregs may be partly due to the reduced ability of DCs to convert non-Treg cells into Tregs. We then explored the in vitro capability of CD4+CD25+ Tregs, either from ITP patients or healthy subjects, to inhibit allogeneic DCs maturation by flow cytometry evaluation of the expression of the costimulatory molecules CD80 and CD86. We demonstrated that in ITP patients CD4+CD25+ Tregs show lower ability to inhibit DCs maturation because they do not affect the expression of CD80 and CD86 molecules. This finding may be related to the lower level of Interleukin-10 and Interleukin-6 in the cocoltures. Taken together, these findings document that the interaction between DCs and Tregs is altered in ITP and suggest that this dysfunction may play a pathogenetic role. Supported in part by BolognaAIL (Italian association against Leukemia, Bologna section) Disclosures: No relevant conflicts of interest to declare.

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