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group_1_presentation_1_-_kidney_transplant_rejection [2016/01/30 00:11] prabahd |
group_1_presentation_1_-_kidney_transplant_rejection [2018/01/25 15:18] (current) |
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| - | <style float-right> | + | <style float-left> |
| - | {{:allorecognition.jpg|}} | + | {{:allorecognition.jpg?300x200}} |
| ''Figure 7: Allorecognition in Renal Transplants'' | ''Figure 7: Allorecognition in Renal Transplants'' | ||
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| Overall, allorecognition leads to the priming of T-cells, activating them to respond to the presenting antigen. In most cases, dendritic cells or other antigen-presenting cells are exposed to these peptides first, resulting in their activation and migration to the thymus. In the thymus, the antigen is presenting via MHC to T-cells, allowing for their maturation and ability to launch an immune response [20]. Recently, it has been elucidated that T-cells do not necessarily need to become activated at the Thymus, but can also be activated directly at the graft via interactions with the endothelial cell lining of the transplant [20]. The microenvironment where T-cells become activated leads to the differentiation of T-cells, varying in their cytokine signatures and functionalities (CD8+ T-cells versus CD4+ T-cells). This differentiation depends on the expression of a master transcription factor, determining the final subset of cytotoxic T-cells (CD8+) and T-helper cells (CD4+). During renal transplants, there are many factors that can affect the microenvironment post-transplant [20]: | Overall, allorecognition leads to the priming of T-cells, activating them to respond to the presenting antigen. In most cases, dendritic cells or other antigen-presenting cells are exposed to these peptides first, resulting in their activation and migration to the thymus. In the thymus, the antigen is presenting via MHC to T-cells, allowing for their maturation and ability to launch an immune response [20]. Recently, it has been elucidated that T-cells do not necessarily need to become activated at the Thymus, but can also be activated directly at the graft via interactions with the endothelial cell lining of the transplant [20]. The microenvironment where T-cells become activated leads to the differentiation of T-cells, varying in their cytokine signatures and functionalities (CD8+ T-cells versus CD4+ T-cells). This differentiation depends on the expression of a master transcription factor, determining the final subset of cytotoxic T-cells (CD8+) and T-helper cells (CD4+). During renal transplants, there are many factors that can affect the microenvironment post-transplant [20]: | ||
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| - | * Immune status of the recipient at the time of transplant | ||
| - | * Degree of ischemia-reperfusion | ||
| - | * Degree of donor-recipient HLA mismatch | ||
| - | * Current immunosuppressive regime | ||
| <style float-right> | <style float-right> | ||
| - | {{:rejection_mech.png|}} | + | {{:rejection_mech.png?300x200}} |
| ''Figure 8: Mechanisms of Rejection'' | ''Figure 8: Mechanisms of Rejection'' | ||
| </style> | </style> | ||
| + | * Immune status of the recipient at the time of transplant | ||
| + | * Degree of ischemia-reperfusion | ||
| + | * Degree of donor-recipient HLA mismatch | ||
| + | * Current immunosuppressive regime | ||
| CD8+ T-cells, also known as cytotoxic T-cells, are typically activated after forming a three-cell cluster between itself, a CD4+ T-cell, and an antigen-presenting cell [20]. It can directly destroy graft cells by expressing perforin to disrupt their membrane and injecting granzyme in to the cell to destroy crucial proteins via the release of cytotoxic granules. FasL released by the cytotoxic T-cell can bind to FasR on the target cell, resulting in the triggering of apoptosis of the graft cell by triggering various cascades [20]. CD4+ T-cells release cytokines that result in inflammation, and can attract other immune cells towards the location of the graft. Recent studies indicate that CD4+ T-cells can result in graft rejection by themselves, although the exact mechanism is not clear [20]. | CD8+ T-cells, also known as cytotoxic T-cells, are typically activated after forming a three-cell cluster between itself, a CD4+ T-cell, and an antigen-presenting cell [20]. It can directly destroy graft cells by expressing perforin to disrupt their membrane and injecting granzyme in to the cell to destroy crucial proteins via the release of cytotoxic granules. FasL released by the cytotoxic T-cell can bind to FasR on the target cell, resulting in the triggering of apoptosis of the graft cell by triggering various cascades [20]. CD4+ T-cells release cytokines that result in inflammation, and can attract other immune cells towards the location of the graft. Recent studies indicate that CD4+ T-cells can result in graft rejection by themselves, although the exact mechanism is not clear [20]. | ||
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| <style float-right> | <style float-right> | ||
| - | {{:fungi.png|}} | + | {{:fungi.png?200x220}} |
| ''Figure 9: Cyclosporine from a Fungal Origin'' | ''Figure 9: Cyclosporine from a Fungal Origin'' | ||
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| <style float-left> | <style float-left> | ||
| - | {{:3d2.png|}} | + | {{:3d2.png?371x265}} |
| ''Figure 10: 3D Print Technology for Customizing Organs'' | ''Figure 10: 3D Print Technology for Customizing Organs'' | ||
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| 3D-Prints is a relatively new application that is being used to print many organs such as the heart, kidneys and other crucial organs <sup>[18]</sup>. | 3D-Prints is a relatively new application that is being used to print many organs such as the heart, kidneys and other crucial organs <sup>[18]</sup>. | ||
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| ====== References ====== | ====== References ====== | ||
