Utilisation de la protéine Tat-Foxp3 pour induire la formation des lymphocytes T régulateurs, dans le contexte de la thérapie cellulaire de la dystrophie musculaire de Duchenne
|Advisor:||Tremblay, Jacques-P.; Skuk, Daniel|
|Abstract:||The Duchenne muscular dystrophy is the most common hereditary muscular disease. This disease is inherited as an X-linked recessive trait. It is caused by the absence of dystrophin in muscle fibers. Cell therapy is the potential treatment but, its success depends on the control of the rejection of the transplanted myoblasts and of the hybrid fibers that they formed. At present, the control of the graft rejection is achieved by administration of powerful immunosuppressive drug. Our long-term aim is to develop a protocol for immune tolerance that would prevent the graft rejection without sustained immunosuppression. The first step of this tolerance protocol that we want to develop is to induce the formation of regulatory T cells using the transcription factor Foxp3. In this study we generated, in bacteria E. coli, a fusion protein Tat-Foxp3. By in vitro assays, we demonstrated that Tat-Foxp3 protein up-regulated the expression of CD25 in naïve CD4+ T cells. Additional experiments will be required to confirm that these CD25 expressing cells are Treg.|
|Document Type:||Mémoire de maîtrise|
|Open Access Date:||19 April 2018|
|Collection:||Thèses et mémoires|
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