review · Journal of Immunology Research
Kidney transplantation serves as the primary treatment for end-stage renal failure, yet graft rejection remains a major obstacle to successful outcomes. Rejection occurs when the recipient immune system recognises the donor kidney as foreign. In particular, human leukocyte antigen mismatches between donors and recipients create substantial complications. These mismatches extend the duration patients spend reliant on dialysis, diminish overall graft survival, and raise patient mortality rates. Exposure to previous transplants, blood transfusions, or pregnancy can sensitise recipients, generating pretransplant antibodies against donor antigens. Additionally, the development of new antibodies after transplantation increases the risk of both acute and chronic organ rejection. Because rejection involves complex interactions between innate and adaptive immune responses, detailed insight into sensitisation mechanisms is vital for refining immunosuppressive strategies and designing targeted therapies.
Kidney transplantation is critical for patients with end-stage renal failure, yet immune rejection severely limits long-term success. Overcoming human leukocyte antigen barriers can shorten the time patients spend dependent on dialysis. Clarifying the biological mechanisms behind immune sensitisation is essential for improving clinical management, refining donor matching, and developing targeted treatments that preserve donor organ function.
This work informs early-stage research into novel immunosuppressive therapies and desensitisation treatments aimed at transplant recipients and clinical immunology teams. Because the abstract describes an overview of immune mechanisms and general future therapeutic directions, it does not detail specific formulated products, clinical trial assets, or near-market technologies.
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Kidney transplantation remains the treatment of choice for end-stage renal failure. When the immune system of the recipient recognizes the transplanted kidney as a foreign object, graft rejection occurs. As part of the host immune defense mechanism, human leukocyte antigen (HLA) is a major challenge for graft rejection in transplantation therapy. The impact of HLA mismatches between the donor and the potential recipient prolongs the time for renal transplantation therapy, tethered to dialysis, latter reduces graft survival, and increases mortality. The formation of pretransplant alloantibodies against HLA class I and II molecules can be sensitized through exposures to blood transfusions, prior transplants, and pregnancy. These preformed HLA antibodies are associated with rejection in kidney transplantation. On the other hand, the development of de novo antibodies may increase the risk for acute and chronic rejections. Allograft rejection results from a complex interplay involving both the innate and the adaptive immune systems. Thus, further insights into the mechanisms of tissue rejection and the risk of HLA sensitization is crucial in developing new therapies that may blunt the immune system against transplanted organs. Therefore, the purpose of this review is to highlight facts about HLA and its sensitization, various mechanisms of allograft rejection, the current immunosuppressive approaches, and the directions for future therapy.
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DOI: 10.1155/2018/5986740
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