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The multifaceted role of complement in kidney transplantation
Skane Univ Hosp, Dept Transplantat, Malmo, Sweden;Lund Univ, Lund, Sweden.
Univ Hosp Ulm, Inst Clin & Expt Traumaimmunol, Ulm, Germany.
Linnaeus Univ, Ctr Biomat Chem, Kalmar, Sweden.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Clinical Immunology. Centre of Biomaterials Chemistry, Linnaeus University, Kalmar, Sweden.
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2018 (English)In: Nature Reviews Nephrology, ISSN 1759-5061, E-ISSN 1759-507X, Vol. 14, no 12, p. 767-781Article, review/survey (Refereed) Published
Abstract [en]

Increasing evidence indicates an integral role for the complement system in the deleterious inflammatory reactions that occur during critical phases of the transplantation process, such as brain or cardiac death of the donor, surgical trauma, organ preservation and ischaemia-reperfusion injury, as well as in humoral and cellular immune responses to the allograft. Ischaemia is the most common cause of complement activation in kidney transplantation and in combination with reperfusion is a major cause of inflammation and graft damage. Complement also has a prominent role in antibody-mediated rejection (ABMR) owing to ABO and HL A incompatibility, which leads to devastating damage to the transplanted kidney. Emerging drugs and treatment modalities that inhibit complement activation at various stages in the complement cascade are being developed to ameliorate the damage caused by complement activation in transplantation. These promising new therapies have various potential applications at different stages in the process of transplantation, including inhibiting the destructive effects of ischaemia and/or reperfusion injury, treating ABMR, inducing accommodation and modulating the adaptive immune response.

Place, publisher, year, edition, pages
Nature Publishing Group, 2018. Vol. 14, no 12, p. 767-781
National Category
Urology and Nephrology Immunology in the medical area
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URN: urn:nbn:se:uu:diva-372949DOI: 10.1038/s41581-018-0071-xISI: 000450235200011PubMedID: 30367174OAI: oai:DiVA.org:uu-372949DiVA, id: diva2:1278800
Funder
Swedish Research Council, 602699Swedish Research Council, 2016-2075-5.1Swedish Research Council, 2016-04519German Research Foundation (DFG), CRC1149 A01Available from: 2019-01-15 Created: 2019-01-15 Last updated: 2019-01-15Bibliographically approved

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Nilsson Ekdahl, KristinaNilsson, Bo

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