Difference between revisions of "Team:CPU CHINA"
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<h5 style="padding: 0px; margin: 5px;">Our HEAD-Treg</h5> | <h5 style="padding: 0px; margin: 5px;">Our HEAD-Treg</h5> | ||
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<h5 style="padding: 0px; margin: 0px;">Description</h5> | <h5 style="padding: 0px; margin: 0px;">Description</h5> | ||
<h4 style="margin: 5px;">Rheumatoid arthritis (RA) is a serious chronic, inflammatory and systemic autoimmune disease. | <h4 style="margin: 5px;">Rheumatoid arthritis (RA) is a serious chronic, inflammatory and systemic autoimmune disease. | ||
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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 | ||
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> | 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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<img class="sponsors" src="https://static.igem.org/mediawiki/2017/d/da/Cyva.jpg"></a> | <img class="sponsors" src="https://static.igem.org/mediawiki/2017/d/da/Cyva.jpg"></a> | ||
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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.
