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Book ; Online: The Role of Complement in Tumors

Rolfe, Barbara / Pio, Ruben / Woodruff, Trent M. / Markiewski, Maciej M. / Manthey, Helga D.

2020

Keywords	Medicine ; Immunology ; complement ; cancer ; metastasis ; C5b-9 ; C1q ; C3a ; C5a ; complement regulatory proteins
Size	1 electronic resource (107 pages)
Publisher	Frontiers Media SA
Document type	Book ; Online
Note	English ; Open Access
HBZ-ID	HT021230763
ISBN	9782889635764 ; 2889635767
Database	ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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Article ; Online: Complement(ing) long-COVID thromboinflammation and pathogenesis.

Lee, John D / Woodruff, Trent M

Trends in immunology

2024

Abstract: The persistence or recurrence of symptoms after acute SARS-CoV-2 infection, termed 'long COVID', presents a formidable challenge to global healthcare systems. Recent research by Cervia-Hasler and colleagues delves into the intricate immunological ... ...

Abstract	The persistence or recurrence of symptoms after acute SARS-CoV-2 infection, termed 'long COVID', presents a formidable challenge to global healthcare systems. Recent research by Cervia-Hasler and colleagues delves into the intricate immunological landscape in patients with long COVID, demonstrating an interplay between complement and coagulation, driven by antiviral antibodies and tissue damage.
Language	English
Publishing date	2024-04-17
Publishing country	England
Document type	Journal Article
ZDB-ID	2036831-8
ISSN	1471-4981 ; 1471-4906
ISSN (online)	1471-4981
ISSN	1471-4906
DOI	10.1016/j.it.2024.04.001
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Article ; Online: Protocol for cell-based screening assay to measure ERK1/2 phosphorylation as a readout for complement receptor activation.

Li, Xaria X / Woodruff, Trent M

STAR protocols

2023 Volume 4, Issue 4, Page(s) 102758

Abstract: The complement receptors C3aR and C5aR1 are promising therapeutic targets. Here, we present a protocol to screen the effects of different agonists and antagonists on these receptors in vitro, using phosphorylated extracellular signal-regulated kinase ( ... ...

Abstract	The complement receptors C3aR and C5aR1 are promising therapeutic targets. Here, we present a protocol to screen the effects of different agonists and antagonists on these receptors in vitro, using phosphorylated extracellular signal-regulated kinase (ERK) as a readout. We describe steps for isolating human monocyte-derived macrophages, culturing and preparing Chinese hamster ovary cells stably expressing human C5aR1 or C3aR, performing pharmacological assays, and detecting phospho-ERK1/2 in the cell lysate. This protocol can also be performed using other cell lines. For complete details on the use and execution of this protocol, please refer to Li et al. (2020)
MeSH term(s)	Cricetinae ; Animals ; Humans ; Phosphorylation ; CHO Cells ; MAP Kinase Signaling System ; Cricetulus ; Receptors, Complement/metabolism
Chemical Substances	Receptors, Complement
Language	English
Publishing date	2023-11-29
Publishing country	United States
Document type	Journal Article
ISSN	2666-1667
ISSN (online)	2666-1667
DOI	10.1016/j.xpro.2023.102758
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Article ; Online: The emerging role of complement in neuromuscular disorders.

Lee, John D / Woodruff, Trent M

Seminars in immunopathology

2021 Volume 43, Issue 6, Page(s) 817–828

Abstract: The complement cascade is a key arm of the immune system that protects the host from exogenous and endogenous toxic stimuli through its ability to potently regulate inflammation, phagocytosis, and cell lysis. Due to recent clinical trial successes and ... ...

Abstract	The complement cascade is a key arm of the immune system that protects the host from exogenous and endogenous toxic stimuli through its ability to potently regulate inflammation, phagocytosis, and cell lysis. Due to recent clinical trial successes and drug approvals for complement inhibitors, there is a resurgence in targeting complement as a therapeutic approach to prevent ongoing tissue destruction in several diseases. In particular, neuromuscular diseases are undergoing a recent focus, with demonstrated links between complement activation and disease pathology. This review aims to provide a comprehensive overview of complement activation and its role during the initiation and progression of neuromuscular disorders including myasthenia gravis, amyotrophic lateral sclerosis, and Duchenne muscular dystrophy. We will review the preclinical and clinical evidence for complement in these diseases, with an emphasis on the complement-targeting drugs in clinical trials for these indications.
MeSH term(s)	Complement Activation ; Complement Inactivating Agents/therapeutic use ; Complement System Proteins ; Humans ; Myasthenia Gravis/drug therapy ; Neuromuscular Diseases/drug therapy ; Neuromuscular Diseases/etiology
Chemical Substances	Complement Inactivating Agents ; Complement System Proteins (9007-36-7)
Language	English
Publishing date	2021-10-27
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2316828-6
ISSN	1863-2300 ; 1863-2297
ISSN (online)	1863-2300
ISSN	1863-2297
DOI	10.1007/s00281-021-00895-4
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Article ; Online: Cell-intrinsic C5a synergizes with Dectin-1 in macrophages to mediate fungal killing.

Li, Xaria X / Fung, Jenny N / Clark, Richard J / Lee, John D / Woodruff, Trent M

Proceedings of the National Academy of Sciences of the United States of America

2024 Volume 121, Issue 5, Page(s) e2314627121

Abstract: The complement factor C5a is a core effector product of complement activation. C5a, acting through its receptors C5aR1 and C5aR2, exerts pleiotropic immunomodulatory functions in myeloid cells, which is vital for host defense against pathogens. Pattern- ... ...

Abstract	The complement factor C5a is a core effector product of complement activation. C5a, acting through its receptors C5aR1 and C5aR2, exerts pleiotropic immunomodulatory functions in myeloid cells, which is vital for host defense against pathogens. Pattern-recognition receptors (PRRs) are similarly expressed by immune cells as detectors of pathogen-associated molecular patterns. Although there is evidence of cross talk between complement and PRR signaling pathways, knowledge of the full potential for C5a-PRR interaction is limited. In this study, we comprehensively investigated how C5a signaling through C5a receptors can modulate diverse PRR-mediated cytokine responses in human primary monocyte-derived macrophages and observed a powerful, concentration-dependent bidirectional effect of C5a on PRR activities. Unexpectedly, C5a synergized with Dectin-1, Mincle, and STING in macrophages to a much greater extent than TLRs. Notably, we also identified that selective Dectin-1 activation using depleted zymosan triggered macrophages to generate cell-intrinsic C5a, which acted on intracellular and cell surface C5aR1, to help sustain mitochondrial ROS generation, up-regulate TNFα production, and enhance fungal killing. This study adds further evidence to the holistic functions of C5a as a central immunomodulator and important orchestrator of pathogen sensing and killing by phagocytes.
MeSH term(s)	Humans ; Complement C5a/metabolism ; Lectins, C-Type/metabolism ; Macrophages/immunology ; Macrophages/metabolism ; Myeloid Cells ; Phagocytes ; Signal Transduction
Chemical Substances	Complement C5a (80295-54-1) ; dectin 1 ; Lectins, C-Type
Language	English
Publishing date	2024-01-22
Publishing country	United States
Document type	Journal Article
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2314627121
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Article ; Online: Complement drives circuit modulation in the adult brain.

Parker, Sandra E / Bellingham, Mark C / Woodruff, Trent M

Progress in neurobiology

2022 Volume 214, Page(s) 102282

Abstract: Once widely considered an immune-privileged organ, the brain is now known to be intimately intertwined with immune-system activation. In particular, the complement system, an enzymatic cascade conferring innate immunity, has crucial functions for several ...

Abstract	Once widely considered an immune-privileged organ, the brain is now known to be intimately intertwined with immune-system activation. In particular, the complement system, an enzymatic cascade conferring innate immunity, has crucial functions for several neurodevelopmental and neuromigratory mechanisms. Recent advances have demonstrated the neurological importance of complement activation in the adult brain, whereby phagocytosis of weakened synapses biologically encodes "forgetting" of information through complement activation. Neurophysiologically, complement factors can also influence the brain's computational processes, increasing neuronal calcium influx and neurotransmitter release and altering synaptic strength. The complement system's effects on synaptic connectivity can also be observed in many pathological conditions including epilepsy, schizophrenia, and viral-induced cognitive deficits, where perturbations of complement-stimulated synaptic remodelling lead to severe dysfunction. In this review we provide an overview of current knowledge for complement in neurodevelopment, and examine recent evidence highlighting a critical physiological role of complement in the plasticity of the adult brain. This is especially relevant due to the explosion of complement-targeted therapeutics in clinical trials to treat neurological disorders.
MeSH term(s)	Brain ; Complement System Proteins ; Epilepsy ; Humans ; Neuronal Plasticity/physiology ; Neurons ; Synapses/pathology
Chemical Substances	Complement System Proteins (9007-36-7)
Language	English
Publishing date	2022-05-06
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	185535-9
ISSN	1873-5118 ; 0301-0082
ISSN (online)	1873-5118
ISSN	0301-0082
DOI	10.1016/j.pneurobio.2022.102282
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Article ; Online: Response to Comment on "Inflammasome inhibition prevents α-synuclein pathology and dopaminergic neurodegeneration in mice".

Albornoz, Eduardo A / Gordon, Richard / Kumar, Vinod / Robertson, Avril A B / Schroder, Kate / Woodruff, Trent M

Science translational medicine

2023 Volume 15, Issue 696, Page(s) eadh0604

Abstract: We have replicated our original finding of elevated cleaved caspase-1 in mouse brains and neuroprotection by an NLRP3 inflammasome inhibitor in two mouse models of Parkinson's disease. ...

Abstract	We have replicated our original finding of elevated cleaved caspase-1 in mouse brains and neuroprotection by an NLRP3 inflammasome inhibitor in two mouse models of Parkinson's disease.
MeSH term(s)	Mice ; Animals ; Inflammasomes ; alpha-Synuclein ; NLR Family, Pyrin Domain-Containing 3 Protein ; Parkinson Disease/pathology ; Dopamine
Chemical Substances	Inflammasomes ; alpha-Synuclein ; NLR Family, Pyrin Domain-Containing 3 Protein ; Dopamine (VTD58H1Z2X)
Language	English
Publishing date	2023-05-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	2518854-9
ISSN	1946-6242 ; 1946-6234
ISSN (online)	1946-6242
ISSN	1946-6234
DOI	10.1126/scitranslmed.adh0604
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Article ; Online: Complement: Bridging the innate and adaptive immune systems in sterile inflammation.

Lo, Martin W / Woodruff, Trent M

Journal of leukocyte biology

2020 Volume 108, Issue 1, Page(s) 339–351

Abstract: The complement system is a collection of soluble and membrane-bound proteins that together act as a powerful amplifier of the innate and adaptive immune systems. Although its role in infection is well established, complement is becoming increasingly ... ...

Abstract	The complement system is a collection of soluble and membrane-bound proteins that together act as a powerful amplifier of the innate and adaptive immune systems. Although its role in infection is well established, complement is becoming increasingly recognized as a key contributor to sterile inflammation, a chronic inflammatory process often associated with noncommunicable diseases. In this context, damaged tissues release danger signals and trigger complement, which acts on a range of leukocytes to augment and bridge the innate and adaptive immune systems. Given the detrimental effect of chronic inflammation, the complement system is therefore well placed as an anti-inflammatory drug target. In this review, we provide a general outline of the sterile activators, effectors, and targets of the complement system and a series of examples (i.e., hypertension, cancer, allograft transplant rejection, and neuroinflammation) that highlight complement's ability to bridge the 2 arms of the immune system.
MeSH term(s)	Adaptive Immunity ; Animals ; Complement System Proteins/immunology ; Graft Rejection/immunology ; Humans ; Immune System/immunology ; Immune System/pathology ; Immunity, Innate ; Inflammation/immunology
Chemical Substances	Complement System Proteins (9007-36-7)
Language	English
Publishing date	2020-03-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	605722-6
ISSN	1938-3673 ; 0741-5400
ISSN (online)	1938-3673
ISSN	0741-5400
DOI	10.1002/JLB.3MIR0220-270R
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Article ; Online: TDP-43 Puts the STING in ALS.

Lee, John D / Woodruff, Trent M

Trends in neurosciences

2020 Volume 44, Issue 2, Page(s) 81–82

Abstract: In a recent study, Yu et al. demonstrated that TAR DNA-binding protein of 43 kDa (TDP-43) causes inflammation in amyotrophic lateral sclerosis (ALS) by triggering mitochondrial (mt)DNA release into the cytoplasm, which subsequently activates the ... ...

Abstract	In a recent study, Yu et al. demonstrated that TAR DNA-binding protein of 43 kDa (TDP-43) causes inflammation in amyotrophic lateral sclerosis (ALS) by triggering mitochondrial (mt)DNA release into the cytoplasm, which subsequently activates the cytoplasmic DNA-sensing cyclic GMP-AMP synthase (cGAS)/stimulator of interferon genes (STING) pathway. These results suggest that inhibition of cGAS/STING could help mitigate inflammation-related neuropathology in ALS.
MeSH term(s)	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine ; Amyotrophic Lateral Sclerosis/genetics ; Bites and Stings ; DNA, Mitochondrial ; DNA-Binding Proteins/genetics ; Humans ; Membrane Proteins/genetics ; Nucleotidyltransferases/metabolism ; Signal Transduction
Chemical Substances	DNA, Mitochondrial ; DNA-Binding Proteins ; Membrane Proteins ; TARDBP protein, human ; 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (9P21XSP91P) ; Nucleotidyltransferases (EC 2.7.7.-)
Language	English
Publishing date	2020-12-20
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	282488-7
ISSN	1878-108X ; 0378-5912 ; 0166-2236
ISSN (online)	1878-108X
ISSN	0378-5912 ; 0166-2236
DOI	10.1016/j.tins.2020.12.001
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Article ; Online: The Complement C5a-C5aR1 GPCR Axis in COVID-19 Therapeutics.

Woodruff, Trent M / Shukla, Arun K

Trends in immunology

2020 Volume 41, Issue 11, Page(s) 965–967

Abstract: The current pandemic of coronavirus disease (COVID-19) caused by SARS-CoV-2 is a significant global health challenge. A recent study by Carvelli and colleagues now demonstrates the involvement of complement C5a and its receptor C5aR1 in disease ... ...

Abstract	The current pandemic of coronavirus disease (COVID-19) caused by SARS-CoV-2 is a significant global health challenge. A recent study by Carvelli and colleagues now demonstrates the involvement of complement C5a and its receptor C5aR1 in disease progression and suggests that blockade of the C5a-C5aR1 axis may represent a potential therapeutic strategy against COVID-19.
MeSH term(s)	Animals ; Antibodies, Monoclonal/immunology ; Antibodies, Monoclonal/pharmacology ; Betacoronavirus/drug effects ; Betacoronavirus/immunology ; Betacoronavirus/physiology ; COVID-19 ; Complement C5a/immunology ; Complement C5a/metabolism ; Coronavirus Infections/immunology ; Coronavirus Infections/therapy ; Coronavirus Infections/virology ; Disease Models, Animal ; Humans ; Pandemics ; Pneumonia, Viral/immunology ; Pneumonia, Viral/therapy ; Pneumonia, Viral/virology ; Receptor, Anaphylatoxin C5a/immunology ; Receptor, Anaphylatoxin C5a/metabolism ; Receptors, G-Protein-Coupled/immunology ; Receptors, G-Protein-Coupled/metabolism ; SARS-CoV-2 ; Signal Transduction/drug effects ; Signal Transduction/immunology
Chemical Substances	Antibodies, Monoclonal ; C5AR1 protein, human ; Receptor, Anaphylatoxin C5a ; Receptors, G-Protein-Coupled ; Complement C5a (80295-54-1)
Keywords	covid19
Language	English
Publishing date	2020-09-23
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2036831-8
ISSN	1471-4981 ; 1471-4906
ISSN (online)	1471-4981
ISSN	1471-4906
DOI	10.1016/j.it.2020.09.008
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