Difference between revisions of "Team:CPU CHINA"

 
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            <p><br>&nbsp;<br></p>
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            <p><br>&nbsp;<br></p>
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            <p><br>&nbsp;<br></p>
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            <center><br>&nbsp;<br></center>
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            <center>
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            <img src="https://static.igem.org/mediawiki/2017/9/97/T--CPU_CHINA--mainpage_new.png" width = "1300">
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            <center class="pagee pagee1">
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            <center><br>&nbsp;<br></center>
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            <p><br>&nbsp;<br></p>
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            <center>
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            <h5>Our HEAD-Treg</h5>
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            <video src="https://static.igem.org/mediawiki/2017/1/14/T--CPU_CHINA--mainpagevideo.mp4" controls="controls" class="video" width = "60%"></video>
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            <h5 style="padding: 0px; margin: 5px;">Our HEAD-Treg</h5>
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            </center>
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            <video src="https://static.igem.org/mediawiki/2017/5/5a/T--CPU_CHINA--V123.mp4" controls="controls" class="video" width = "55%"></video>
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            <center class="pagee pagee2">
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        <center><br><br>&nbsp;<br><br></center>
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                <p><br>&nbsp;<br></p>
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            <center>
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            <p><br>&nbsp;<br></p>
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             <h3>Description</h3>
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             <h5 style="padding: 0px; margin: 0px;">Description</h5>
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             <h4><br>Rheumatoid arthritis (RA) is a serious chronic, inflammatory and systemic autoimmune disease.
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             <h4 style="margin: 5px;">Rheumatoid arthritis (RA) is a serious chronic, inflammatory and systemic autoimmune disease.
 
                 <br>It is of great essence to develop a novel cell-targeted therapy for RA  
 
                 <br>It is of great essence to develop a novel cell-targeted therapy for RA  
 
because there is no radical cure
 
because there is no radical cure
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               <br>Meanwhile, we insert the Syn-Notch receptor to activate the functional stability pathway of Tregs in the
 
               <br>Meanwhile, we insert the Syn-Notch receptor to activate the functional stability pathway of Tregs in the
 
                     inflammatory environment, which enables them to play their role of immunosuppression in lesions more
 
                     inflammatory environment, which enables them to play their role of immunosuppression in lesions more
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                     efficiently and more stably. <br>These two redirections of the two different but interrelated systems on Tregs ensure this novel therapy a promising anti-RA effect. </h4></center>
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                     efficiently and more stably. <br>These two redirections of the two different but interrelated systems on Tregs ensure this novel therapy a promising anti-RA effect. </h4>
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             </div>
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                          <p><br>&nbsp;<br></p>
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<center class="footer-left">
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  <p class="footer-links" style="text-align:center;">
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<a target="_blank" href="https://www.cpu.edu.cn">
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Latest revision as of 03:20, 2 November 2017


 


 


 


 

Our HEAD-Treg


 


 

Description

Rheumatoid arthritis (RA) is a serious chronic, inflammatory and systemic autoimmune disease.
It is of great essence to develop a novel cell-targeted therapy for RA because there is no radical cure for RA for the time being.
To solve the problems existing in the current treatment of RA, we design and build a brand new immunotherapy.
FOXP3+ regulatory T cells(Tregs), which can suppress and regulate immune reactions, are modified
utilizing a lentiviral vector system to express a chimeric antigen receptor(CAR) targeting inflammatory cells associated with RA.
Meanwhile, we insert the Syn-Notch receptor to activate the functional stability pathway of Tregs in the inflammatory environment, which enables them to play their role of immunosuppression in lesions more efficiently and more stably.
These two redirections of the two different but interrelated systems on Tregs ensure this novel therapy a promising anti-RA effect.