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Journal of Zhejiang University SCIENCE B 1998 Vol.-1 No.-1 P.

http://doi.org/10.1631/jzus.B2300947


OX40L promotes follicular helper T cell differentiation and function in mice with immune thrombocytopenia


Author(s):  Ziyin YANG, Lei HAI, Xiaoyu CHEN, Siwen WU, Yan LV, Dawei CUI, Jue XIE

Affiliation(s):  Department of Blood Transfusion, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, China

Corresponding email(s):   daweicui@zju.edu.cn, zyyyxj2011@zju.edu.cn

Key Words:  OX40L, OX40, Immune thrombocytopenia, Follicular T helper cell, B cell


Ziyin YANG, Lei HAI, Xiaoyu CHEN, Siwen WU, Yan LV, Dawei CUI, Jue XIE. OX40L promotes follicular helper T cell differentiation and function in mice with immune thrombocytopenia[J]. Journal of Zhejiang University Science B, 1998, -1(-1): .

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author="Ziyin YANG, Lei HAI, Xiaoyu CHEN, Siwen WU, Yan LV, Dawei CUI, Jue XIE",
journal="Journal of Zhejiang University Science B",
volume="-1",
number="-1",
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year="1998",
publisher="Zhejiang University Press & Springer",
doi="10.1631/jzus.B2300947"
}

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%T OX40L promotes follicular helper T cell differentiation and function in mice with immune thrombocytopenia
%A Ziyin YANG
%A Lei HAI
%A Xiaoyu CHEN
%A Siwen WU
%A Yan LV
%A Dawei CUI
%A Jue XIE
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T1 - OX40L promotes follicular helper T cell differentiation and function in mice with immune thrombocytopenia
A1 - Ziyin YANG
A1 - Lei HAI
A1 - Xiaoyu CHEN
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A1 - Yan LV
A1 - Dawei CUI
A1 - Jue XIE
J0 - Journal of Zhejiang University Science B
VL - -1
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PB - Zhejiang University Press & Springer
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DOI - 10.1631/jzus.B2300947


Abstract: 
immune thrombocytopenia (ITP) is a hemorrhagic autoimmune disease characterized by antibody-mediated platelet injury. ITP has complicated immunopathological mechanisms that need further elucidation. It is well known that the costimulatory molecules OX40L%29&ck%5B%5D=abstract&ck%5B%5D=keyword'>OX40L and OX40 play essential roles in the immunological mechanisms of autoimmune diseases. Previously, we discovered that the expression of OX40L%29&ck%5B%5D=abstract&ck%5B%5D=keyword'>OX40L and OX40 is significantly increased in the PBMCs of ITP patients. In our present study, OX40L%29&ck%5B%5D=abstract&ck%5B%5D=keyword'>OX40L-induced Tfh cells exhibited an activated phenotype with elevated ICOS, PD-1, and CD40L expression in vitro. Moreover, aberrant OX40L%29&ck%5B%5D=abstract&ck%5B%5D=keyword'>OX40L-OX40 expression might promote the Tfh1-to-Tfh2 shift in vivo, inducing the generation of autoantibodies by enhancing the helper function of Tfh cells for B lymphocytes in a mouse model, which might accelerate the progression of ITP. Additionally, signal transduction through the OX40L%29&ck%5B%5D=abstract&ck%5B%5D=keyword'>OX40L-OX40 axis might be related to the activation of TRAF-NF-κB and JAK-STAT signaling pathways. Overall, OX40L%29&ck%5B%5D=abstract&ck%5B%5D=keyword'>OX40L-OX40 signaling is proposed as a potential novel therapeutic target for ITP.

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