Abstract
A transplant between two people who are not genetically identical is called an allotransplant and the process is called allotransplantation. Donor organs and tissues can be from people who are living, or people who have died because of a significant brain injury or lack of circulation. Allotransplantation can create a rejection process where the immune system of the recipient attacks the foreign donor organ or tissue and destroys it. The recipient may need to take immunosuppressive medication for the rest of their life to reduce the risk of rejection of the donated organ. In general, deliberately induced immunosuppression is performed to prevent the body from rejecting an organ transplant. The adverse effects associated with these agents and the risks of long-term immunosuppression present a number of challenges for the clinician. Immune tolerance, or immunological tolerance, or immunotolerance, is a state of unresponsiveness of the immune system to substances or tissue that have the capacity to elicit an immune response in a given organism.
Highlights
A transplant between two people who are not genetically identical is called an allotransplant and the process is called allotransplantation
Solid organ transplantation is a life-saving procedure for various end-stage diseases, but the inherent requirement for life-long immunsuppression for preventing graft rejection comes with many side effects, such as increased risk of infection, neoplasms as well as nephrotoxicity and diabetogenicity [1,2,3,4]
IL-10-generated human tolerogenic DCs were optimal in producing highly suppressive Tregs [59]. — TAIC is an immunoregulatory macrophage. They are IFNg-stimulated monocyte-derived cells (IFNg-MdC) described as a nonDC and more mature form of resting macrophage expres sing F4/80, CD11, CD86, PDL-1. Their suppressive effect is through the enrichment of CD4+CD25+FoxP3 cells and cell contact-and caspase-dependent depletion of activated T cells [60]. — Mesenchymal stromal cells (MSCs) have immunomodulatory properties, they inhibit T cell activation and proliferation possibly due to the production of nitric oxi de and IDO [61]
Summary
There are two obligatory components to achieving transplantation tolerance: depletion of alloreactive Tconv and upregulation of alloreactive Treg cells. The balance between graft destruction and regulation can be shifted using stra tegies to inhibit the activity of Tconv cells and/or increase the relative frequency or functional activity of alloantigenreactive Treg cells. Mixed chimeric and cellular tolerogenic therapies are being trialed where drug-based therapies have failed [21, 22]. Manipulating innate immune system TLRs drive innate immune responses as part of I-R (ischemia-reperfusion) injury and this leads to the subsequent initiation of adaptive alloimmune responses; so deficiency in the TLR adaptor protein MyD88 leads to donor antigen-specific tolerance. MyD88 deficiency is associated with an altered balance of Tregs over Tconv cells promoting tolerance instead of rejection
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