Ficolin-1 Is Present in a Highly Mobilizable Subset of Human Neutrophil Granules and Associates with the Cell Surface after Stimulation with fMLP.

Roervig, Sara; Honoré, Christian; Larsson, Lars‐Inge; Ohlsson, Sophie; Pedersen, Claus; Jacobsen, Lars C.; Cowland, Jack B.; Garred, Peter; Borregaard, Niels

doi:10.1182/blood.v112.11.1267.1267

Cited by 21 publications

(43 citation statements)

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“…104 Ficolin-1 is believed to primarily exert its function on site during inflammation where it can get secreted by monocytes/macrophages and granulocytes; the latter appear to be the major source and reservoir of ficolin-1. 109,110 It is noteworthy that ficolin-1 is tethered to the membranes of the cells secreting it. 14,110,111 Ficolin-1 is also present in serum, although in relatively low levels with an average concentration of 0.3 μg/ml.…”

Section: Tissue Distributionmentioning

confidence: 99%

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A journey through the lectin pathway of complement—MBL and beyond

Garred

Genster

Pilely

et al. 2016

Immunological Reviews

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328

302

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Mannose-binding lectin (MBL), collectin-10, collectin-11, and the ficolins (ficolin-1, ficolin-2, and ficolin-3) are soluble pattern recognition molecules in the lectin complement pathway. These proteins act as mediators of host defense and participate in maintenance of tissue homeostasis. They bind to conserved pathogen-specific structures and altered self-antigens and form complexes with the pentraxins to modulate innate immune functions. All molecules exhibit distinct expression in different tissue compartments, but all are found to a varying degree in the circulation. A common feature of these molecules is their ability to interact with a set of serine proteases named MASPs (MASP-1, MASP-2, and MASP-3). MASP-1 and -2 trigger the activation of the lectin pathway and MASP-3 may be involved in the activation of the alternative pathway of complement. Furthermore, MASPs mediate processes related to coagulation, bradykinin release, and endothelial and platelet activation. Variant alleles affecting expression and structure of the proteins have been associated with a variety of infectious and non-infectious diseases, most commonly as disease modifiers. Notably, the severe 3MC (Malpuech, Michels, Mingarelli, and Carnevale) embryonic development syndrome originates from rare mutations affecting either collectin-11 or MASP-3, indicating a broader functionality of the complement system than previously anticipated. This review summarizes the characteristics of the molecules in the lectin pathway.

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Section: Tissue Distributionmentioning

confidence: 99%

“…109,110 It is noteworthy that ficolin-1 is tethered to the membranes of the cells secreting it. 14,110,111 Ficolin-1 is also present in serum, although in relatively low levels with an average concentration of 0.3 μg/ml. 112 FCN2 is expressed in the liver 96,104 and the average serum concentration of ficolin-2 is 5 μg/ml.…”

Section: Tissue Distributionmentioning

confidence: 99%

A journey through the lectin pathway of complement—MBL and beyond

Garred

Genster

Pilely

et al. 2016

Immunological Reviews

Self Cite

328

302

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“…25 Granules containing gelatinase and ficolin-1, termed ficolin-1-rich granules, are proposed as a separate granule subset. 20,26 Only 30 of 1123 proteins are maximally expressed in gelatinase granules, however, while 246 of 1193 proteins are maximally expressed in ficolin-rich granules. 20 The small number of proteins maximally expressed in gelatinase granules suggests a limited value in separating gelatinase granules and ficolin-rich granules.…”

Section: Granulopoiesis and Granule Contentsmentioning

confidence: 99%

Therapeutic targeting of neutrophil exocytosis

Catz

McLeish

2020

Journal of Leukocyte Biology

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Dysregulation of neutrophil activation causes disease in humans. Neither global inhibition of neutrophil functions nor neutrophil depletion provides safe and/or effective therapeutic approaches. The role of neutrophil granule exocytosis in multiple steps leading to recruitment and cell injury led each of our laboratories to develop molecular inhibitors that interfere with specific molecular regulators of secretion. This review summarizes neutrophil granule formation and contents, the role granule cargo plays in neutrophil functional responses and neutrophil‐mediated diseases, and the mechanisms of granule release that provide the rationale for development of our exocytosis inhibitors. We present evidence for the inhibition of granule exocytosis in vitro and in vivo by those inhibitors and summarize animal data indicating that inhibition of neutrophil exocytosis is a viable therapeutic strategy.

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“…Ficolin-1 is predominantly synthesized by myeloid cells and is a major content of granules in PMNs, and is secreted from activated monocytes and neutrophils. 56,57 It is found in serum with a mean concentration of 0.3-0.5 μg/mL. 58 Ficolin-2 is synthesized in the liver with a mean serum concentration of 5 μg/mL, 59 and ficolin-3 is synthesized in the lung and liver with a mean serum concentration of 25 μg/mL.…”

Section: Complementmentioning

confidence: 99%

Dangerous liaisons: complement, coagulation, and kallikrein/kinin cross‐talk act as a linchpin in the events leading to thromboinflammation

Ekdahl

Teramura

Hamad

et al. 2016

Immunological Reviews

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131

127

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Innate immunity is fundamental to our defense against microorganisms. Physiologically, the intravascular innate immune system acts as a purging system that identifies and removes foreign substances leading to thromboinflammatory responses, tissue remodeling, and repair. It is also a key contributor to the adverse effects observed in many diseases and therapies involving biomaterials and therapeutic cells/organs. The intravascular innate immune system consists of the cascade systems of the blood (the complement, contact, coagulation, and fibrinolytic systems), the blood cells (polymorphonuclear cells, monocytes, platelets), and the endothelial cell lining of the vessels. Activation of the intravascular innate immune system in vivo leads to thromboinflammation that can be activated by several of the system's pathways and that initiates repair after tissue damage and leads to adverse reactions in several disorders and treatment modalities. In this review, we summarize the current knowledge in the field and discuss the obstacles that exist in order to study the cross-talk between the components of the intravascular innate immune system. These include the use of purified in vitro systems, animal models and various types of anticoagulants. In order to avoid some of these obstacles we have developed specialized human whole blood models that allow investigation of the cross-talk between the various cascade systems and the blood cells. We in particular stress that platelets are involved in these interactions and that the lectin pathway of the complement system is an emerging part of innate immunity that interacts with the contact/coagulation system. Understanding the resulting thromboinflammation will allow development of new therapeutic modalities.

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Ficolin-1 Is Present in a Highly Mobilizable Subset of Human Neutrophil Granules and Associates with the Cell Surface after Stimulation with fMLP.

Cited by 21 publications

References 0 publications

A journey through the lectin pathway of complement—MBL and beyond

A journey through the lectin pathway of complement—MBL and beyond

Therapeutic targeting of neutrophil exocytosis

Dangerous liaisons: complement, coagulation, and kallikrein/kinin cross‐talk act as a linchpin in the events leading to thromboinflammation

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