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The multifaceted role of complement in kidney transplantation
Skåne University Hospital;Lund University.
Univ Hosp Ulm, Germany.
Linnaeus University, Faculty of Health and Life Sciences, Department of Chemistry and Biomedical Sciences. (Linnaeus Ctr Biomat Chem, BMC)ORCID iD: 0000-0002-9301-1977
Linnaeus University, Faculty of Health and Life Sciences, Department of Chemistry and Biomedical Sciences. Uppsala University. (Linnaeus Ctr Biomat Chem, BMC)ORCID iD: 0000-0001-7888-1571
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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
Immunology
Research subject
Biomedical Sciences, Immunology
Identifiers
URN: urn:nbn:se:lnu:diva-78998DOI: 10.1038/s41581-018-0071-xISI: 000450235200011PubMedID: 30367174Scopus ID: 2-s2.0-85055731914OAI: oai:DiVA.org:lnu-78998DiVA, id: diva2:1268583
Funder
Swedish Research Council, 602699; 2016-2075-5.1; 2016-04519
Note

Other funding  agencies:

Deutsche Forschungsgemeinschaft (DFG): CRC1149 A01 

Available from: 2018-12-06 Created: 2018-12-06 Last updated: 2020-06-05Bibliographically approved

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Mohlin, CamillaNilsson Ekdahl, Kristina

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