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<h2><span class="sd">HEAD-Treg</span> </h2> <h2>Human Engineered Anti-Autoimmune-Disease Regulatory T Cells System</h2> | <h2><span class="sd">HEAD-Treg</span> </h2> <h2>Human Engineered Anti-Autoimmune-Disease Regulatory T Cells System</h2> | ||
<h3 class="ar-title">Abstract</h3> | <h3 class="ar-title">Abstract</h3> | ||
− | <h4><br>FOXP3 + regulatory T cells (Treg) are a class of T lymphocyte subsets that play an immunosuppressive and regulatory function. The dysfunction of FOXP3 + Treg is closely related to the development of autoimmune diseases, such as rheumatoid arthritis. FOXP3, a transcription factor in Forkhead family, whose functional stability is regulated by post-translational modification enzymes, is a key transcription factor for Treg cells’ specific expression. The ubiquitinase USP7 was able to specifically modify the FOXP3 protein by specific ubiquitination to enhance the functional stability of FOXP3, thereby enhancing the immunosuppressive function of Treg cells. </h4> | + | <h4><br>FOXP3+ regulatory T cells (Treg) are a class of T lymphocyte subsets that play an immunosuppressive and regulatory function. The dysfunction of FOXP3+ Treg is closely related to the development of autoimmune diseases, such as rheumatoid arthritis. FOXP3, a transcription factor in Forkhead family, whose functional stability is regulated by post-translational modification enzymes, is a key transcription factor for Treg cells’ specific expression. The ubiquitinase USP7 was able to specifically modify the FOXP3 protein by specific ubiquitination to enhance the functional stability of FOXP3, thereby enhancing the immunosuppressive function of Treg cells. </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 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> |
Revision as of 13:48, 1 November 2017