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<h4><br>In different tissues, the proportion of different types of CD4+ lymphocytes, to a large extent, is determined by various cytokines that can induce the differentiation of CD4+ CD45RA+ naive T cells. For example, IL-12 leads to Th1 cells, Il-4 leads to Th2 cells and TGF-β leads to Treg cells. Many studies have also shown that subgroups of helper T cells such as Th1, Th2, Th17, and Treg, which have been differentiated into functional subpopulations, can also be transdifferentiated into other subgroups of helper T cells under the action of certain cytokines. Their original functions may decline if transdifferentiation does not happen in some conditions. <h4> | <h4><br>In different tissues, the proportion of different types of CD4+ lymphocytes, to a large extent, is determined by various cytokines that can induce the differentiation of CD4+ CD45RA+ naive T cells. For example, IL-12 leads to Th1 cells, Il-4 leads to Th2 cells and TGF-β leads to Treg cells. Many studies have also shown that subgroups of helper T cells such as Th1, Th2, Th17, and Treg, which have been differentiated into functional subpopulations, can also be transdifferentiated into other subgroups of helper T cells under the action of certain cytokines. Their original functions may decline if transdifferentiation does not happen in some conditions. <h4> | ||
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− | <h4><br>In order to theoretically demonstrate that regulatory T cells are dysfunctional or transdifferentiated in the cell microenvironment of rheumatoid arthritis patients imbued with a large number of inflammatory factors, and to describe the necessity of intervening the corresponding regulatory pathway of Treg cells in the clinical treatment of rheumatoid arthritis, we established the mathematical model of T cell differentiation and transdifferentiation (see more from Model section).</h4> | + | <h4><br>In order to theoretically demonstrate that regulatory T cells are dysfunctional or transdifferentiated in the cell microenvironment of rheumatoid arthritis patients imbued with a large number of inflammatory factors, and to describe the necessity of intervening the corresponding regulatory pathway of Treg cells in the clinical treatment of rheumatoid arthritis, we established the mathematical model of T cell differentiation and transdifferentiation (see more from <a href="https://2017.igem.org/Team:CPU_CHINA/Model">Model section</a>).</h4> |
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− | <h4><br> | + | <h4><br>Based on our mathematical model analysis, we can theoretically come to the conclusion that in patients with rheumatoid arthritis, due to the secretion of inflammatory cytokines, the T cell differentiation to functional effector T cells will be promoted and meanwhile the function of regulatory T cells will be further weakened. We can also learn that regulatory T cells cannot survive in too intensive inflammatory environment in the bodies of rheumatoid arthritis patients. In the light of all conclusions of the mathematical model analysis, our design ideas for the treatment of rheumatoid arthritis has become clearer: enhance the stability of regulatory T cells in the presence of inflammatory cytokines by inserting our new system, thereby blocking inflammation the occurrence of dysfunction and transdifferentiation of Treg cells. Finally, we established the following intervention strategy (Figure 5).</h4> |
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<center><img src="https://static.igem.org/mediawiki/2017/d/d8/T--CPU_CHINA--eng-figure3_3.png" width = "800"></center> | <center><img src="https://static.igem.org/mediawiki/2017/d/d8/T--CPU_CHINA--eng-figure3_3.png" width = "800"></center> |
Revision as of 18:16, 1 November 2017