Difference between revisions of "Team:CPU CHINA"

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             <img src="https://static.igem.org/mediawiki/2017/9/97/T--CPU_CHINA--mainpage_new.png" width = "1300">
 
             <img src="https://static.igem.org/mediawiki/2017/9/97/T--CPU_CHINA--mainpage_new.png" width = "1300">
 
             </center>
 
             </center>
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            <h5>Our HEAD-Treg</h5>
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             <center class="page page2">
 
             <center class="page page2">
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            <h5>Our HEAD-Treg</h5>
 
             <video src="https://static.igem.org/mediawiki/2017/1/14/T--CPU_CHINA--mainpagevideo.mp4" controls="controls" class="video" width = "60%"></video>
 
             <video src="https://static.igem.org/mediawiki/2017/1/14/T--CPU_CHINA--mainpagevideo.mp4" controls="controls" class="video" width = "60%"></video>
 
             </center>
 
             </center>
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            <center class="page page3"><h3>Description</h3></center>
 
  
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              <center> <h4><br>Rheumatoid arthritis (RA) is a serious chronic, inflammatory and systemic autoimmune disease.
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            <center class="page page3"><h3>Description</h3>
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            <h4><br>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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            </center>
  
 
         </div>
 
         </div>

Revision as of 12:04, 1 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.