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Article ; Online: Correction to: Complement in ischaemia-reperfusion injury and transplantation.

Howard, Mark C / Nauser, Christopher L / Farrar, Conrad A / Sacks, Steven H

2022 Volume 44, Issue 3, Page(s) 391

Language	English
Publishing date	2022-03-18
Publishing country	Germany
Document type	Published Erratum
ZDB-ID	2316828-6
ISSN	1863-2300 ; 1863-2297
ISSN (online)	1863-2300
ISSN	1863-2297
DOI	10.1007/s00281-022-00924-w
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Article ; Online: Complement in ischaemia-reperfusion injury and transplantation.

Howard, Mark C / Nauser, Christopher L / Farrar, Conrad A / Sacks, Steven H

Seminars in immunopathology

2021 Volume 43, Issue 6, Page(s) 789–797

Abstract: Until recently, the only known condition in which complement could mediate transplant injury was the rare occurrence of antibody-mediated rejection, in which the original concept of antibody immunity against the transplant was supported by complementary ... ...

Abstract	Until recently, the only known condition in which complement could mediate transplant injury was the rare occurrence of antibody-mediated rejection, in which the original concept of antibody immunity against the transplant was supported by complementary proteins present in the serum. This has changed within the last two decades because of evidence that the processes of ischaemia-reperfusion injury followed by T cell-mediated rejection are also critically dependent on components generated by the complement system. We now have a clearer understanding of the complement triggers and effectors that mediate injury, and a detailed map of their local sites of production and activation in the kidney. This is providing helpful guidelines as to how these harmful processes that restrict transplant outcomes can be targeted for therapeutic benefit. Here we review some of the recent advances highlighting relevant therapeutic targets.
MeSH term(s)	Complement Activation ; Complement System Proteins ; Graft Rejection ; Humans ; Kidney Transplantation/adverse effects ; Reperfusion Injury/etiology
Chemical Substances	Complement System Proteins (9007-36-7)
Language	English
Publishing date	2021-11-10
Publishing country	Germany
Document type	Journal Article ; Review
ZDB-ID	2316828-6
ISSN	1863-2300 ; 1863-2297
ISSN (online)	1863-2300
ISSN	1863-2297
DOI	10.1007/s00281-021-00896-3
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Article ; Online: Complement Recognition Pathways in Renal Transplantation.

Nauser, Christopher L / Farrar, Conrad A / Sacks, Steven H

Journal of the American Society of Nephrology : JASN

2017 Volume 28, Issue 9, Page(s) 2571–2578

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 ... ...

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.
MeSH term(s)	Adaptive Immunity ; Animals ; Collectins/immunology ; Collectins/metabolism ; Complement Pathway, Classical ; Complement System Proteins/immunology ; Complement System Proteins/metabolism ; Graft Rejection/immunology ; Humans ; Kidney Transplantation ; Lectins/immunology ; Lectins/metabolism ; Mannose-Binding Lectin/immunology ; Mannose-Binding Lectin/metabolism ; Reperfusion Injury/immunology
Chemical Substances	Colec11 protein, human ; Collectins ; Lectins ; Mannose-Binding Lectin ; Complement System Proteins (9007-36-7)
Language	English
Publishing date	2017-06-29
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1085942-1
ISSN	1533-3450 ; 1046-6673
ISSN (online)	1533-3450
ISSN	1046-6673
DOI	10.1681/ASN.2017010079
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Article ; Online: Structural and functional diversity of collectins and ficolins and their relationship to disease.

Howard, Mark / Farrar, Conrad A / Sacks, Steven H

Seminars in immunopathology

2017 Volume 40, Issue 1, Page(s) 75–85

Abstract: Pattern recognition molecules are sensors for the innate immune system and trigger a number of pathophysiological functions after interaction with the corresponding ligands on microorganisms or altered mammalian cells. Of those pattern recognition ... ...

Abstract	Pattern recognition molecules are sensors for the innate immune system and trigger a number of pathophysiological functions after interaction with the corresponding ligands on microorganisms or altered mammalian cells. Of those pattern recognition molecules used by the complement system, collagen-like lectins (collectins) are an important subcomponent. Whereas the best known of these collectins, mannose-binding lectin, largely occurs as a circulating protein following production by hepatocytes, the most recently described collectins exhibit strong local biosynthesis. This local production and release of soluble collectin molecules appear to serve local tissue functions at extravascular sites, including a developmental function. In this article, we focus on the characteristics of collectin-11 (CL-11 or CL-K1), whose ubiquitous expression and multiple activities likely reflect a wide biological relevance. Collectin-11 appears to behave as an acute phase protein whose production associated with metabolic and physical stress results in locally targeted inflammation and tissue cell death. Early results indicate the importance of fucosylated ligand marking the injured cells targeted by collectin-11, and we suggest that further characterisation of this and related ligands will lead to better understanding of pathophysiological significance and exploitation for clinical benefit.
MeSH term(s)	Animals ; Collectins/chemistry ; Collectins/metabolism ; Complement Activation/immunology ; Complement System Proteins/immunology ; Complement System Proteins/metabolism ; Disease Susceptibility/immunology ; Host-Pathogen Interactions/immunology ; Humans ; Immunity, Innate ; Lectins/chemistry ; Lectins/metabolism ; Polysaccharides/chemistry ; Polysaccharides/metabolism ; Protein Binding ; Receptors, Pattern Recognition/metabolism ; Signal Transduction ; Structure-Activity Relationship ; Ficolins
Chemical Substances	Collectins ; Lectins ; Polysaccharides ; Receptors, Pattern Recognition ; Complement System Proteins (9007-36-7)
Language	English
Publishing date	2017-09-11
Publishing country	Germany
Document type	Journal Article ; Review
ZDB-ID	2316828-6
ISSN	1863-2300 ; 1863-2297
ISSN (online)	1863-2300
ISSN	1863-2297
DOI	10.1007/s00281-017-0642-0
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Article ; Online: Mechanisms of rejection: role of complement.

Farrar, Conrad A / Sacks, Steven H

Current opinion in organ transplantation

2013 Volume 19, Issue 1, Page(s) 8–13

Abstract: Purpose of review: To provide the reader with an up-to-date comprehensive review of recent findings that highlight advances describing how proteins of the complement cascades contribute to the pathogenesis of solid organ rejection. The review is ... ...

Abstract	Purpose of review: To provide the reader with an up-to-date comprehensive review of recent findings that highlight advances describing how proteins of the complement cascades contribute to the pathogenesis of solid organ rejection. The review is focussed mainly on renal transplantation. Recent findings: Of note are recent advances in elucidating the interactions between anaphylatoxins and their receptors in organ transplantation; there is evidence of direct engagement of C5aR on donor tubules and in addition, mechanisms by which the allostimulatory capacity of dendritic cells is modulated by complement are more fully understood. Activation of the lectin pathway is increasingly implicated in allograft rejection and the role of complement in modulating regulatory T cells is being vigorously investigated. As an alternative to systemic complement inhibition, there is continued focus on the design of targeted anti-complement therapies, directed to the donor organ. Summary: Complement has evolved as the first line of defence against pathogens, employing well defined effector mechanisms to rapidly remove infectious material. However, complement effector mechanisms are also triggered during inflammation associated with solid organ transplantation. Hence, complement has a significant role in mediating donor organ injury during both the initial ischaemia/reperfusion phase and the subsequent adaptive immune responses. Research on mechanisms of complement-mediated injury in transplantation provide a basis for the development of therapies that are aimed at transiently blocking complement activation at the site of injury, whereas leaving systemic anti-bacterial complement effector mechanisms intact.
MeSH term(s)	Anaphylatoxins/immunology ; Animals ; Complement Activation ; Complement System Proteins/immunology ; Graft Rejection/immunology ; Humans ; Kidney Transplantation ; Transplantation Immunology
Chemical Substances	Anaphylatoxins ; Complement System Proteins (9007-36-7)
Language	English
Publishing date	2013-12-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1390429-2
ISSN	1531-7013 ; 1087-2418
ISSN (online)	1531-7013
ISSN	1087-2418
DOI	10.1097/MOT.0000000000000037
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Article ; Online: Role of the lectin complement pathway in kidney transplantation.

Farrar, Conrad A / Zhou, Wuding / Sacks, Steven H

Immunobiology

2016 Volume 221, Issue 10, Page(s) 1068–1072

Abstract: In the last 15 years two major advances in the role of complement in the kidney transplant have come about. The first is that ischaemia reperfusion injury and its profound effect on transplant outcome is dependent on the terminal product of complement ... ...

Abstract	In the last 15 years two major advances in the role of complement in the kidney transplant have come about. The first is that ischaemia reperfusion injury and its profound effect on transplant outcome is dependent on the terminal product of complement activation, C5b-9. The second key observation relates to the function of the small biologically active fragments C3a and C5a released by complement activation in increasing antigen presentation and priming the T cell response that results in transplant rejection. In both cases local synthesis of C3 principally by the renal tubule cells plays an essential role that overshadows the role of the circulating pool of C3 generated largely by hepatocyte synthesis. More recent efforts have investigated the molecules expressed by renal tissue that can trigger complement activation. These have revealed a prominent effect of collectin-11 (CL-11), a soluble C-type lectin that is expressed in renal tissue and aligns with its major ligand L-fucose at sites of complement activation following ischaemic stress. Biochemical studies have shown that interaction between CL-11 and L-fucose results in complement activation by the lectin complement pathway, precisely targeting the innate immune response to the ischaemic tubule surface. Therapeutic approaches to reduce inflammatory and immune stimulation in ischaemic kidney have so far targeted C3 or its activation products and several are in clinical trials. The finding that lectin-fucose interaction is an important trigger of lectin pathway complement activation within the donor organ opens up further therapeutic targets where intervention could protect the donor kidney against complement.
MeSH term(s)	Animals ; Biomarkers ; Complement Pathway, Mannose-Binding Lectin/immunology ; Complement System Proteins/immunology ; Complement System Proteins/metabolism ; Graft Rejection/immunology ; Humans ; Immunity, Innate ; Kidney Transplantation ; Mannose-Binding Lectin/immunology ; Mannose-Binding Lectin/metabolism ; Reperfusion Injury/etiology ; Reperfusion Injury/metabolism ; Reperfusion Injury/pathology ; Transplantation Immunology
Chemical Substances	Biomarkers ; Mannose-Binding Lectin ; Complement System Proteins (9007-36-7)
Language	English
Publishing date	2016-05-24
Publishing country	Netherlands
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	563292-4
ISSN	1878-3279 ; 0171-2985
ISSN (online)	1878-3279
ISSN	0171-2985
DOI	10.1016/j.imbio.2016.05.004
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Article ; Online: l-Fucose prevention of renal ischaemia/reperfusion injury in Mice.

Howard, Mark C / Nauser, Christopher L / Farrar, Conrad A / Wallis, Russell / Sacks, Steven H

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

2019 Volume 34, Issue 1, Page(s) 822–834

Abstract: In a recent study, we identified a fucosylated damage-associated ligand exposed by ischemia on renal tubule epithelial cells, which after recognition by collectin-11 (CL-11 or collectin kidney 1 (CL-K1)), initiates complement activation and acute kidney ... ...

Abstract	In a recent study, we identified a fucosylated damage-associated ligand exposed by ischemia on renal tubule epithelial cells, which after recognition by collectin-11 (CL-11 or collectin kidney 1 (CL-K1)), initiates complement activation and acute kidney injury. We exploited the ability to increase the local tissue concentration of free l-fucose following systemic administration, in order to block ligand binding by local CL-11 and prevent complement activation. We achieved a thirty-five-fold increase in the intrarenal concentration of l-fucose following an IP bolus given before the ischemia induction procedure - a concentration found to significantly block in vitro binding of CL-11 on hypoxia-stressed renal tubule cells. At this l-fucose dose, complement activation and acute post-ischemic kidney injury are prevented, with additional protection achieved by a second bolus after the induction procedure. CL-11
MeSH term(s)	Acute Kidney Injury/drug therapy ; Acute Kidney Injury/metabolism ; Animals ; Complement Activation/drug effects ; Complement System Proteins/drug effects ; Complement System Proteins/metabolism ; Fucose/metabolism ; Fucose/pharmacokinetics ; Graft Survival/drug effects ; Ischemia/drug therapy ; Ischemia/metabolism ; Kidney/drug effects ; Kidney/metabolism ; Kidney Transplantation/methods ; Mice, Knockout ; Reperfusion Injury/drug therapy ; Reperfusion Injury/metabolism
Chemical Substances	Fucose (28RYY2IV3F) ; Complement System Proteins (9007-36-7)
Language	English
Publishing date	2019-11-27
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639186-2
ISSN	1530-6860 ; 0892-6638
ISSN (online)	1530-6860
ISSN	0892-6638
DOI	10.1096/fj.201901582R
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Article ; Online: Rationale for targeting complement in COVID-19.

Polycarpou, Anastasia / Howard, Mark / Farrar, Conrad A / Greenlaw, Roseanna / Fanelli, Giorgia / Wallis, Russell / Klavinskis, Linda S / Sacks, Steven

EMBO molecular medicine

2020 Volume 12, Issue 8, Page(s) e12642

Abstract: A novel coronavirus, SARS-CoV-2, has recently emerged in China and spread internationally, posing a health emergency to the global community. COVID-19 caused by SARS-CoV-2 is associated with an acute respiratory illness that varies from mild to the life- ... ...

Abstract	A novel coronavirus, SARS-CoV-2, has recently emerged in China and spread internationally, posing a health emergency to the global community. COVID-19 caused by SARS-CoV-2 is associated with an acute respiratory illness that varies from mild to the life-threatening acute respiratory distress syndrome (ARDS). The complement system is part of the innate immune arsenal against pathogens, in which many viruses can evade or employ to mediate cell entry. The immunopathology and acute lung injury orchestrated through the influx of pro-inflammatory macrophages and neutrophils can be directly activated by complement components to prime an overzealous cytokine storm. The manifestations of severe COVID-19 such as the ARDS, sepsis and multiorgan failure have an established relationship with activation of the complement cascade. We have collected evidence from all the current studies we are aware of on SARS-CoV-2 immunopathogenesis and the preceding literature on SARS-CoV-1 and MERS-CoV infection linking severe COVID-19 disease directly with dysfunction of the complement pathways. This information lends support for a therapeutic anti-inflammatory strategy against complement, where a number of clinically ready potential therapeutic agents are available.
MeSH term(s)	Adult ; Alveolar Epithelial Cells/immunology ; Alveolar Epithelial Cells/metabolism ; Alveolar Epithelial Cells/virology ; Angiotensin-Converting Enzyme 2 ; Animals ; Betacoronavirus/physiology ; COVID-19 ; Child ; Complement Activation/drug effects ; Complement C3b/antagonists & inhibitors ; Complement C3b/physiology ; Complement Inactivating Agents/pharmacology ; Complement Inactivating Agents/therapeutic use ; Coronavirus Infections/drug therapy ; Coronavirus Infections/immunology ; Cytokine Release Syndrome/drug therapy ; Cytokine Release Syndrome/etiology ; Cytokine Release Syndrome/immunology ; Glycosylation ; Humans ; Immunity, Innate ; Ligands ; Mice ; Models, Animal ; Models, Molecular ; Pandemics ; Pattern Recognition, Automated ; Peptidyl-Dipeptidase A/metabolism ; Pneumonia, Viral/drug therapy ; Pneumonia, Viral/immunology ; Protein Conformation ; Protein Processing, Post-Translational ; Receptors, Virus/metabolism ; Respiratory Distress Syndrome/etiology ; Respiratory Distress Syndrome/immunology ; SARS-CoV-2 ; Spike Glycoprotein, Coronavirus/chemistry ; Spike Glycoprotein, Coronavirus/metabolism ; COVID-19 Drug Treatment
Chemical Substances	Complement Inactivating Agents ; Ligands ; Receptors, Virus ; Spike Glycoprotein, Coronavirus ; spike protein, SARS-CoV-2 ; Complement C3b (80295-43-8) ; Peptidyl-Dipeptidase A (EC 3.4.15.1) ; ACE2 protein, human (EC 3.4.17.23) ; Ace2 protein, mouse (EC 3.4.17.23) ; Angiotensin-Converting Enzyme 2 (EC 3.4.17.23)
Keywords	covid19
Language	English
Publishing date	2020-07-12
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2467145-9
ISSN	1757-4684 ; 1757-4676
ISSN (online)	1757-4684
ISSN	1757-4676
DOI	10.15252/emmm.202012642
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Article ; Online: Collectin-11 (CL-11) Is a Major Sentinel at Epithelial Surfaces and Key Pattern Recognition Molecule in Complement-Mediated Ischaemic Injury.

Nauser, Christopher L / Howard, Mark C / Fanelli, Giorgia / Farrar, Conrad A / Sacks, Steven

Frontiers in immunology

2018 Volume 9, Page(s) 2023

Abstract: The complement system is a dynamic subset of the innate immune system, playing roles in host defense, clearance of immune complexes and cell debris, and priming the adaptive immune response. Over the last 40 years our understanding of the complement ... ...

Abstract	The complement system is a dynamic subset of the innate immune system, playing roles in host defense, clearance of immune complexes and cell debris, and priming the adaptive immune response. Over the last 40 years our understanding of the complement system has evolved from identifying its presence and recognizing its role in the blood to now focusing on understanding the role of local complement synthesis in health and disease. In particular, the local synthesis of complement was found to have an involvement in mediating ischaemic injury, including following transplantation. Recent work on elucidating the triggers of local complement synthesis and activation in renal tissue have led to the finding that Collectin-11 (CL-11) engages with L-fucose at the site of ischaemic stress, namely at the surface of the proximal tubular epithelial cells. What remains unknown is the precise structure of the damage-associated ligand that participates in CL-11 binding and subsequent complement activation. In this article, we will discuss our hypothesis regarding the role of CL-11 as an integral tissue-based pattern recognition molecule which we postulate has a significant contributory role in complement-mediated ischaemic injury.
MeSH term(s)	Animals ; Collectins/metabolism ; Complement Activation ; Complement System Proteins/metabolism ; Epithelial Cells/physiology ; Humans ; Ischemia/immunology ; Kidney/metabolism ; Kidney/pathology ; Kidney Transplantation ; Receptors, Pattern Recognition/metabolism
Chemical Substances	Colec11 protein, human ; Collectins ; Receptors, Pattern Recognition ; Complement System Proteins (9007-36-7)
Language	English
Publishing date	2018-09-06
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2018.02023
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Article ; Online: Control of innate immunological mechanisms as a route to drug minimization.

Asgari, Elham / Farrar, Conrad A / Sacks, Steven H

Current opinion in organ transplantation

2014 Volume 19, Issue 4, Page(s) 342–347

Abstract: Purpose of review: Much research in transplantation focuses on treatments for rejection and induction of tolerance. Recent evidence has shown that initial inflammation induced by innate immune effectors after transplantation has a key role in modulating ...

Abstract	Purpose of review: Much research in transplantation focuses on treatments for rejection and induction of tolerance. Recent evidence has shown that initial inflammation induced by innate immune effectors after transplantation has a key role in modulating adaptive immune responses that cause organ rejection. Here, we describe the role of the innate immune system, particularly the complement activation pathways, and how they influence adaptive immune responses post-transplantation and current strategies, which are under development to block these innate pathways. Recent findings: Anaphylatoxins and their respective receptors are proving to be important in T-cell-mediated immunity and make attractive targets for therapies designed to promote tolerance in solid organ transplantation. Additionally, regulators of complement activation are currently being tested in clinical trials, with improvements in drug delivery. Summary: Preventing ischaemia-reperfusion injury in transplanted organs significantly reduces immune activation and promotes graft survival. Research into the mechanisms of complement activation in both native organ ischaemia and transplantation models detail emerging roles for complement intermediates that can serve as targets for intervention, with the aim of reducing early post-transplant inflammation, reducing the intensity of immunosuppressive regimens, leading to prolonged graft survival.
MeSH term(s)	Animals ; Complement Activation/immunology ; Complement System Proteins/immunology ; Complement System Proteins/physiology ; Graft Rejection/immunology ; Graft Rejection/prevention & control ; Humans ; Immunity, Cellular/immunology ; Immunity, Innate ; Immunosuppressive Agents/therapeutic use ; Reperfusion Injury/immunology ; Reperfusion Injury/prevention & control
Chemical Substances	Immunosuppressive Agents ; Complement System Proteins (9007-36-7)
Language	English
Publishing date	2014-05-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1390429-2
ISSN	1531-7013 ; 1087-2418
ISSN (online)	1531-7013
ISSN	1087-2418
DOI	10.1097/MOT.0000000000000094
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