TengjieCPU (Talk | contribs) |
TengjieCPU (Talk | contribs) |
||
Line 47: | Line 47: | ||
<h4><br>In patients with rheumatoid arthritis, the balance between Th17 and Treg is usually broken, and inflammatory cells such as Th17 predominate in the human body. A number of inflammatory cytokines, such as IL-17A, IL-6 and TNF-α and so on, secreted by Th17 and other inflammatory cells enhance the inflammation of the lesion, which causes the local enrichment of effector cells such as CD20+ B lymphocytes in the focus and deprives the normal function of Treg cells, resulting in further decline in immunosuppressive capacity. Based on these facts, we hope that our cell therapy program that is to isolate and obtain primary regulatory T cells from rheumatoid arthritis patients and then reinfute engineered Treg cells to the human body, can have a promising effect in the treatment of rheumatism.</h4> | <h4><br>In patients with rheumatoid arthritis, the balance between Th17 and Treg is usually broken, and inflammatory cells such as Th17 predominate in the human body. A number of inflammatory cytokines, such as IL-17A, IL-6 and TNF-α and so on, secreted by Th17 and other inflammatory cells enhance the inflammation of the lesion, which causes the local enrichment of effector cells such as CD20+ B lymphocytes in the focus and deprives the normal function of Treg cells, resulting in further decline in immunosuppressive capacity. Based on these facts, we hope that our cell therapy program that is to isolate and obtain primary regulatory T cells from rheumatoid arthritis patients and then reinfute engineered Treg cells to the human body, can have a promising effect in the treatment of rheumatism.</h4> | ||
− | <h4><br>In our design, first, we designed a SynNotch system that contains a modified Notch protein capable of specifically activating the gene expression of USP7 in inflammatory conditions with the presence of IL17A. USP7 proteins can lead to de-ubiquitination of the FOXP3 protein, so that enhance the stability of FOXP3 protein in the inflammation environment by protecting FOXP3 from degradation via ubiquitination. As a result, Treg cells can maintain their immunosuppressive function. Meantime, we designed a CAR system that | + | <h4><br>In our design, first, we designed a SynNotch system that contains a modified Notch protein capable of specifically activating the gene expression of USP7 in inflammatory conditions with the presence of IL17A. USP7 proteins can lead to de-ubiquitination of the FOXP3 protein, so that enhance the stability of FOXP3 protein in the inflammation environment by protecting FOXP3 from degradation via ubiquitination. As a result, Treg cells can maintain their immunosuppressive function. Meantime, we designed a CAR system that enabled Treg cells to target CD20+ B lymph Cell specifically to play an immunosuppressive function and thus play an anti-inflammatory effect. </h4> |
<h4><br>Given our design and purpose, we call the system a Human Engineered Anti-Autoimmune-Disease Regulatory T Cells System (HEAD-Treg).</h4> | <h4><br>Given our design and purpose, we call the system a Human Engineered Anti-Autoimmune-Disease Regulatory T Cells System (HEAD-Treg).</h4> |
Revision as of 15:25, 1 November 2017