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Article ; Online: Factor VII-Activating Protease: Hemostatic Protein or Immune Regulator?

Zeerleder, Sacha

2017 Volume 44, Issue 2, Page(s) 151–158

Abstract: Factor VII (FVII)-activating protease (FSAP) is a serine protease in plasma, which was initially described to play a role in coagulation by activation of FVII, independent of tissue factor, and in fibrinolysis by cleavage of single-chain urokinase. ... ...

Abstract	Factor VII (FVII)-activating protease (FSAP) is a serine protease in plasma, which was initially described to play a role in coagulation by activation of FVII, independent of tissue factor, and in fibrinolysis by cleavage of single-chain urokinase. Recent studies, however, suggest that FSAP-mediated FVII cleavage is negligible and that FSAP may exert procoagulant functions via cleavage of tissue factor pathway inhibitor. Meanwhile, many substrates of FSAP have been identified, such as platelet-derived growth factor, basic fibroblast growth factor/epidermal growth factor, histones, and high-molecular-weight kininogen. FSAP has also shown to induce DNA released from dead cells. Given its propensity for autoproteolysis and degradation, studies on the activation and regulation of FSAP are difficult to perform. Recent animal studies suggest a role of FSAP in the pathogenesis of arteriosclerosis, vascular integrity and probably also in the regulation of coagulation initiation. This review will focus on the biochemical properties of FSAP, regulation of FSAP activation, and finally its role in vascular disease and acute systemic inflammatory diseases, such as sepsis.
MeSH term(s)	Factor VII/immunology ; Hemostasis/physiology ; Humans
Chemical Substances	Factor VII (9001-25-6)
Language	English
Publishing date	2017-11-24
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	196901-8
ISSN	1098-9064 ; 0094-6176
ISSN (online)	1098-9064
ISSN	0094-6176
DOI	10.1055/s-0037-1607431
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Article: Immunoglobulin-Substitutionstherapie bei hämatologischen Patienten mit sekundärem Antikörpermangel.

Braschler, Thomas R / Zeerleder, Sacha

Therapeutische Umschau. Revue therapeutique

2021 Volume 79, Issue 6, Page(s) 295–300

Abstract: Immunglobulin Substitution Therapy in Hematological Patients with secondary Antibody ... ...

Title translation	Immunglobulin Substitution Therapy in Hematological Patients with secondary Antibody Deficiency.
Abstract	Immunglobulin Substitution Therapy in Hematological Patients with secondary Antibody Deficiency
MeSH term(s)	Humans ; Immunologic Deficiency Syndromes/diagnosis ; Immunologic Deficiency Syndromes/drug therapy
Language	German
Publishing date	2021-10-30
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	82044-1
ISSN	1664-2864 ; 0040-5930
ISSN (online)	1664-2864
ISSN	0040-5930
DOI	10.1024/0040-5930/a001364
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Article: Factor VII-Activating Protease: Hemostatic Protein or Immune Regulator?

Zeerleder, Sacha

Seminars in Thrombosis and Hemostasis

(Extrahemostatic Functions of Platelets and Coagulation Factors)

2017 Volume 44, Issue 02, Page(s) 151–158

Series title	Extrahemostatic Functions of Platelets and Coagulation Factors
Abstract	Factor VII (FVII)-activating protease (FSAP) is a serine protease in plasma, which was initially described to play a role in coagulation by activation of FVII, independent of tissue factor, and in fibrinolysis by cleavage of single-chain urokinase. Recent studies, however, suggest that FSAP-mediated FVII cleavage is negligible and that FSAP may exert procoagulant functions via cleavage of tissue factor pathway inhibitor. Meanwhile, many substrates of FSAP have been identified, such as platelet-derived growth factor, basic fibroblast growth factor/epidermal growth factor, histones, and high-molecular-weight kininogen. FSAP has also shown to induce DNA released from dead cells. Given its propensity for autoproteolysis and degradation, studies on the activation and regulation of FSAP are difficult to perform. Recent animal studies suggest a role of FSAP in the pathogenesis of arteriosclerosis, vascular integrity and probably also in the regulation of coagulation initiation. This review will focus on the biochemical properties of FSAP, regulation of FSAP activation, and finally its role in vascular disease and acute systemic inflammatory diseases, such as sepsis.
Keywords	factor VII-activating protease ; inflammation ; hyaluronic acid binding protein 2 ; nucleosomes ; C1-inhibitor ; PAI-1 ; tissue factor pathway inhibitor
Language	English
Publishing date	2017-11-24
Publisher	Thieme Medical Publishers
Publishing place	Stuttgart ; New York
Document type	Article
ZDB-ID	196901-8
ISSN	1098-9064 ; 0094-6176
ISSN (online)	1098-9064
ISSN	0094-6176
DOI	10.1055/s-0037-1607431
Database	Thieme publisher's database

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Article ; Online: It takes two to thrombosis: Hemolysis and complement.

Delvasto-Nuñez, Laura / Jongerius, Ilse / Zeerleder, Sacha

Blood reviews

2021 Volume 50, Page(s) 100834

Abstract: Thromboembolic events represent the most common complication of hemolytic anemias characterized by complement-mediated hemolysis such as paroxysmal nocturnal hemoglobinuria and autoimmune hemolytic anemia. Similarly, atypical hemolytic uremic syndrome is ...

Abstract	Thromboembolic events represent the most common complication of hemolytic anemias characterized by complement-mediated hemolysis such as paroxysmal nocturnal hemoglobinuria and autoimmune hemolytic anemia. Similarly, atypical hemolytic uremic syndrome is characterized by hemolysis and thrombotic abnormalities. The main player in the development of thrombosis in hemolytic diseases is suggested to be the complement system. However, the release of extracellular hemoglobin and heme by hemolysis itself can also drive procoagulant responses. Both, complement activation and hemolysis promote the activation of neutrophils resulting in the formation of neutrophil extracellular traps and induce inflammation and vascular damage which all together might (synergistically) lead to hypercoagulability. In this review we aim to summarize the current knowledge on the role of complement activation and hemolysis in the onset of thrombosis in hemolytic diseases. This review will discuss the interplay between different biological systems and neutrophil activation contributing to the pathogenesis of thrombosis. Finally, we will combine this fundamental knowledge and address the pathophysiology of hemolysis in prototypical complement-driven diseases.
MeSH term(s)	Atypical Hemolytic Uremic Syndrome ; Complement Activation ; Hemoglobinuria, Paroxysmal/blood ; Hemoglobinuria, Paroxysmal/complications ; Hemolysis ; Humans ; Thrombosis/blood ; Thrombosis/etiology
Language	English
Publishing date	2021-04-30
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	639015-8
ISSN	1532-1681 ; 0268-960X
ISSN (online)	1532-1681
ISSN	0268-960X
DOI	10.1016/j.blre.2021.100834
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Article ; Online: Heme oxygenase-1: Equally important in allogeneic hematopoietic stem cell transplantation and organ transplantation?

Verheij, Myrddin / Zeerleder, Sacha / Voermans, Carlijn

Transplant immunology

2021 Volume 68, Page(s) 101419

Abstract: The intracellular enzyme heme oxygenase-1 (HO-1) is responsible for the degradation of cell-free (cf) heme. Cfheme, released upon cell damage and cell death from hemoglobin, mitochondria and myoglobin, functions as a powerful damage-associated molecular ... ...

Abstract	The intracellular enzyme heme oxygenase-1 (HO-1) is responsible for the degradation of cell-free (cf) heme. Cfheme, released upon cell damage and cell death from hemoglobin, mitochondria and myoglobin, functions as a powerful damage-associated molecular pattern (DAMP). Indeed, cfheme plays a role in a myriad of diseases characterized by (systemic) inflammation, and its rapid degradation by HO-1 is pivotal to maintain homeostasis. In the past decade, HO-1 has been extensively studied for its potential protective role in different transplantation settings, including allogeneic hematopoietic stem cell transplantation (HSCT), solid organ transplantation and pancreatic islet transplantation. These studies have shown that HO-1 can be induced by a wide range of molecules, and that induction of HO-1 has the potential to significantly reduce the incidence and severity of transplantation-related complications such as graft-versus-host disease (GvHD) and ischemia/reperfusion injury (IRI). As such, further investigation into the use of HO-1-inducing agents in human transplantation settings to facilitate the potential use of these agents in the clinic is warranted. In this review, we summarize the literature of the past 10 years on the role of HO-1 in allogeneic HSCT, solid organ transplantation (focusing on kidney and liver) and pancreatic islet transplantation. Furthermore, we provide a hypothesis about the way that HO-1 is able to provide protection against acute GvHD after allogeneic HSCT. A total of 48 research articles and 17 review articles were included in this review.
MeSH term(s)	Graft vs Host Disease ; Hematopoietic Stem Cell Transplantation ; Heme Oxygenase-1 ; Humans ; Organ Transplantation ; Reperfusion Injury
Chemical Substances	Heme Oxygenase-1 (EC 1.14.14.18)
Language	English
Publishing date	2021-06-02
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1160846-8
ISSN	1878-5492 ; 0966-3274
ISSN (online)	1878-5492
ISSN	0966-3274
DOI	10.1016/j.trim.2021.101419
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Article: Hemotherapy with New Blood Products.

Korte, Wolfgang / Zeerleder, Sacha S

Transfusion medicine and hemotherapy : offizielles Organ der Deutschen Gesellschaft fur Transfusionsmedizin und Immunhamatologie

2018 Volume 45, Issue 2, Page(s) 84

Language	English
Publishing date	2018-03-28
Publishing country	Switzerland
Document type	Editorial
ZDB-ID	2100848-6
ISSN	1660-3818 ; 1660-3796
ISSN (online)	1660-3818
ISSN	1660-3796
DOI	10.1159/000488379
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Article ; Online: Autoimmune haemolytic anaemia - a practical guide to cope with a diagnostic and therapeutic challenge.

Zeerleder, S

The Netherlands journal of medicine

2011 Volume 69, Issue 4, Page(s) 177–184

Abstract: Autoimmune haemolytic anaemia (AIHA) is a rare disease. In clinical practice, diagnosis and treatment of AIHA turns out to be troublesome. Correct diagnosis is dependent on proper comprehension of the pathophysiology and the laboratory tests performed by ...

Abstract	Autoimmune haemolytic anaemia (AIHA) is a rare disease. In clinical practice, diagnosis and treatment of AIHA turns out to be troublesome. Correct diagnosis is dependent on proper comprehension of the pathophysiology and the laboratory tests performed by the transfusion laboratory. The present review provides a short overview on the pathogenesis of autoimmune haemolytic anaemia. The diagnostic pitfalls will be discussed and a diagnostic algorithm for proper diagnosis of AI HA will be given. Moreover, a brief overview on the treatment of different forms of AIHA is given.
MeSH term(s)	Adrenal Cortex Hormones/therapeutic use ; Anemia, Hemolytic, Autoimmune/diagnosis ; Anemia, Hemolytic, Autoimmune/drug therapy ; Anemia, Hemolytic, Autoimmune/immunology ; Autoantibodies/blood ; Blood Transfusion ; Cytotoxins/therapeutic use ; Humans ; Immunoglobulin A/blood ; Immunoglobulin G/blood ; Immunoglobulin M/blood
Chemical Substances	Adrenal Cortex Hormones ; Autoantibodies ; Cytotoxins ; Immunoglobulin A ; Immunoglobulin G ; Immunoglobulin M
Language	English
Publishing date	2011-04
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	193149-0
ISSN	1872-9061 ; 0300-2977
ISSN (online)	1872-9061
ISSN	0300-2977
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Article ; Online: C1-inhibitor: more than a serine protease inhibitor.

Zeerleder, Sacha

Seminars in thrombosis and hemostasis

2011 Volume 37, Issue 4, Page(s) 362–374

Abstract: C1-inhibitor (C1-inh) is a crucial regulator of the activation of plasmatic cascade systems involved in inflammation contributing to the homeostasis in the generation of proinflammatory mediators. The importance of C1-inh is illustrated by patients with ... ...

Abstract	C1-inhibitor (C1-inh) is a crucial regulator of the activation of plasmatic cascade systems involved in inflammation contributing to the homeostasis in the generation of proinflammatory mediators. The importance of C1-inh is illustrated by patients with hereditary angioedema where decreased levels of C1-inh lead to an uncontrolled generation of vasoactive peptides resulting in potential life-threatening subcutaneous edema. Recent publications, however, suggest that the anti-inflammatory properties of C1-inh do not strictly depend on its capacity to regulate the complement and contact phase system. This review summarizes the biochemical characteristics of C1-inh and its role in the regulation of plasmatic cascade systems as well as the role of the nonserpin domain.
MeSH term(s)	Animals ; Complement C1 Inhibitor Protein/chemistry ; Complement C1 Inhibitor Protein/physiology ; Fibrinolysis/physiology ; Humans
Chemical Substances	Complement C1 Inhibitor Protein
Language	English
Publishing date	2011-06
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	196901-8
ISSN	1098-9064 ; 0094-6176
ISSN (online)	1098-9064
ISSN	0094-6176
DOI	10.1055/s-0031-1276585
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Article ; Online: Correlation of Peripheral Chimeric Antigen Receptor T-cell (CAR-T Cell) mRNA Expression Levels with Toxicities and Outcomes in Patients with Diffuse Large B-cell Lymphoma

Messerli, Christian / Wiedemann, Gertrud / Porret, Naomi / Nagler, Michael / Seipel, Katja / Jeker, Barbara / Novak, Urban / Zeerleder, Sacha / Bacher, Ulrike / Pabst, Thomas

Turkish journal of haematology : official journal of Turkish Society of Haematology

2023 Volume 40, Issue 3, Page(s) 187–196

Abstract: Cytokine-release syndrome (CRS) and immune effector cell-associated neurotoxicity syndrome (ICANS) are significant complications in patients with relapsed/refractory diffuse large B-cell lymphoma undergoing chimeric antigen receptor T-cell (CAR-T cell) ... ...

Abstract	Cytokine-release syndrome (CRS) and immune effector cell-associated neurotoxicity syndrome (ICANS) are significant complications in patients with relapsed/refractory diffuse large B-cell lymphoma undergoing chimeric antigen receptor T-cell (CAR-T cell) therapy. However, it remains unclear whether CAR-T cell expression itself is clinically relevant. We assessed CAR-T cell mRNA expression and DNA concentration by digital droplet PCR in peripheral blood from 14 sequential CAR-T cell recipients. Patients were grouped according to CAR-T cell peak expression. Patients with high CAR-T cell peak expression (8 patients; 57%) had higher rates of ICANS (p=0.0308) and intensive care unit admission (p=0.0404), longer durations of hospitalization (p=0.0077), and, although not statistically significant, a higher rate of CRS (p=0.0778). There was a correlation of CAR-T cell mRNA expression with DNA concentration, but CAR-T cell expression levels failed to correlate to response or survival. Our data suggest that higher CAR-T cell peak mRNA expression is associated with increased risk for ICANS and possibly CRS, requiring further investigation in larger studies.
MeSH term(s)	Humans ; T-Lymphocytes ; Receptors, Chimeric Antigen/genetics ; Lymphoma, Large B-Cell, Diffuse/genetics ; Lymphoma, Large B-Cell, Diffuse/therapy ; Immunotherapy, Adoptive/adverse effects ; RNA, Messenger/genetics
Chemical Substances	cell-associated neurotoxicity ; Receptors, Chimeric Antigen ; RNA, Messenger
Language	English
Publishing date	2023-07-31
Publishing country	Turkey
Document type	Journal Article
ZDB-ID	2185903-6
ISSN	1308-5263 ; 1300-7777
ISSN (online)	1308-5263
ISSN	1300-7777
DOI	10.4274/tjh.galenos.2023.2023.0136
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Article ; Online: Mechanisms of haemolysis-induced kidney injury.

Van Avondt, Kristof / Nur, Erfan / Zeerleder, Sacha

Nature reviews. Nephrology

2019 Volume 15, Issue 11, Page(s) 671–692

Abstract: Intravascular haemolysis is a fundamental feature of chronic hereditary and acquired haemolytic anaemias, including those associated with haemoglobinopathies, complement disorders and infectious diseases such as malaria. Destabilization of red blood ... ...

Abstract	Intravascular haemolysis is a fundamental feature of chronic hereditary and acquired haemolytic anaemias, including those associated with haemoglobinopathies, complement disorders and infectious diseases such as malaria. Destabilization of red blood cells (RBCs) within the vasculature results in systemic inflammation, vasomotor dysfunction, thrombophilia and proliferative vasculopathy. The haemoprotein scavengers haptoglobin and haemopexin act to limit circulating levels of free haemoglobin, haem and iron - potentially toxic species that are released from injured RBCs. However, these adaptive defence systems can fail owing to ongoing intravascular disintegration of RBCs. Induction of the haem-degrading enzyme haem oxygenase 1 (HO1) - and potentially HO2 - represents a response to, and endogenous defence against, large amounts of cellular haem; however, this system can also become saturated. A frequent adverse consequence of massive and/or chronic haemolysis is kidney injury, which contributes to the morbidity and mortality of chronic haemolytic diseases. Intravascular destruction of RBCs and the resulting accumulation of haemoproteins can induce kidney injury via a number of mechanisms, including oxidative stress and cytotoxicity pathways, through the formation of intratubular casts and through direct as well as indirect proinflammatory effects, the latter via the activation of neutrophils and monocytes. Understanding of the detailed pathophysiology of haemolysis-induced kidney injury offers opportunities for the design and implementation of new therapeutic strategies to counteract the unfavourable and potentially fatal effects of haemolysis on the kidney.
MeSH term(s)	Acute Kidney Injury/etiology ; Animals ; Heme/adverse effects ; Hemolysis ; Humans
Chemical Substances	Heme (42VZT0U6YR)
Language	English
Publishing date	2019-08-27
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2490366-8
ISSN	1759-507X ; 1759-5061
ISSN (online)	1759-507X
ISSN	1759-5061
DOI	10.1038/s41581-019-0181-0
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