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J Am Soc Nephrol. 2017 Sep;28(9):2571-2578. doi: 10.1681/ASN.2017010079. Epub 2017 Jun 29.

Complement Recognition Pathways in Renal Transplantation.

Author information

1
Medical Research Council Centre for Transplantation, Division of Transplantation Immunology and Mucosal Biology, King's College London, National Health Service Guy's and St. Thomas' Trust, London, United Kingdom christopher.nauser@kcl.ac.uk.
2
Medical Research Council Centre for Transplantation, Division of Transplantation Immunology and Mucosal Biology, King's College London, National Health Service Guy's and St. Thomas' Trust, London, United Kingdom.

Abstract

The complement system, consisting of soluble and cell membrane-bound components of the innate immune system, has defined roles in the pathophysiology of renal allograft rejection. Notably, the unavoidable ischemia-reperfusion injury inherent to transplantation is mediated through the terminal complement activation products C5a and C5b-9. Furthermore, biologically active fragments C3a and C5a, produced during complement activation, can modulate both antigen presentation and T cell priming, ultimately leading to allograft rejection. Earlier work identified renal tubule cell synthesis of C3, rather than hepatic synthesis of C3, as the primary source of C3 driving these effects. Recent efforts have focused on identifying the local triggers of complement activation. Collectin-11, a soluble C-type lectin expressed in renal tissue, has been implicated as an important trigger of complement activation in renal tissue. In particular, collectin-11 has been shown to engage L-fucose at sites of ischemic stress, activating the lectin complement pathway and directing the innate immune response to the distressed renal tubule. The interface between collectin-11 and L-fucose, in both the recipient and the allograft, is an attractive target for therapies intended to curtail renal inflammation in the acute phase.

KEYWORDS:

collectin-11; complement; lectin pathway; renal transplantation

PMID:
28663231
PMCID:
PMC5576943
DOI:
10.1681/ASN.2017010079
[Indexed for MEDLINE]
Free PMC Article

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