Monoclonal antibody 2C5 specifically targets neutrophil extracellular traps

Mendes, Lívia Palmerston; Rostamizadeh, Kobra; Gollomp, Kandace; Myerson, Jacob W.; Marcos‐Contreras, Oscar A.; Zamora, Marco; Luther, Ed; Brenner, J.; Filipczak, Nina; Li, Xiang; Torchilin, Vladimir P.

doi:10.1080/19420862.2020.1850394

Cited by 7 publications

(3 citation statements)

References 55 publications

(77 reference statements)

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“…Whether ACPA will also protect against and/or ameliorate disease in other models is currently not known. Likewise, the mechanisms underlying the protective effects mediated by ACPA are not fully elucidated, but current data point to a requirement to bind to the inhibitory FcgRIIB on macrophages as well as on the ability of ACPA to inhibit neutrophil-mediated Netosis, thereby reducing the “tissue Neutrophil Extracellular Trap burden” resulting in an anti-inflammatory effect [44 ▪▪ ,47 ▪▪ ]. Understanding the mechanisms responsible for the ACPA-induced improvement of (neutrophil-dependent?)…”

Section: Recent Antimodified Protein Antibody Developmentsmentioning

confidence: 99%

Autoantibodies in rheumatoid arthritis – rheumatoid factor, anticitrullinated protein antibodies and beyond

Steiner,

Toes

2024

Current Opinion in Rheumatology

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Purpose of review RA is characterized by the presence of autoantibodies among which rheumatoid factors (RFs) and antimodified protein antibodies (AMPA) are serological hallmarks of the disease. In recent years, several novel insights into the biology, immunogenetics and clinical relevance of these autoantibodies have been obtained, which deserve to be discussed in more detail. Recent findings RFs from RA patients seem to target distinct epitopes which appear to be quite specific for RA. Determination of immunoglobulin A (IgA) isotypes of RF and anticitrullinated protein antibodies (ACPA) may provide prognostic information because their presence is associated with reduced therapeutic responses to TNF inhibitors. Furthermore, IgA levels are increased in RA patients and IgA immune complexes are more potent than immunoglobulin G (IgG) complexes in inducing NET formation. Concerning AMPAs, investigations on variable domain glycosylation (VDG) revealed effects on antigen binding and activation of autoreactive B cells. Studies on pathogenetic involvement of ACPA suggest Janus-faced roles: on the one hand, ACPA may be involved in joint destruction and pain perception while on the other hand protective anti-inflammatory effects may be attributed to a subset of ACPAs. Summary The autoimmune response in RA is extremely complex and still far from being fully understood. Antibodies are not only valuable diagnostic biomarkers but also seem to play pivotal roles in the pathophysiology of RA.

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Section: Recent Antimodified Protein Antibody Developmentsmentioning

confidence: 99%

Autoantibodies in rheumatoid arthritis – rheumatoid factor, anticitrullinated protein antibodies and beyond

Steiner,

Toes

2024

Current Opinion in Rheumatology

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“…215 The micellated monoclonal antibody 2C5 is specific to the intact nucleosome of NETs and can also be used to deliver DNase I aimed at NETs to treat inflammation. 218,225…”

Section: Nanodelivery Systemsmentioning

confidence: 99%

Role and Therapeutic Targeting Strategies of Neutrophil Extracellular Traps in Inflammation

Li,

Xiao,

Filipczak

et al. 2023

IJN

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Neutrophil extracellular traps (NETs) are large DNA reticular structures secreted by neutrophils and decorated with histones and antimicrobial proteins. As a key mechanism for neutrophils to resist microbial invasion, NETs play an important role in the killing of microorganisms (bacteria, fungi, and viruses). Although NETs are mostly known for mediating microbial killing, increasing evidence suggests that excessive NETs induced by stimulation of physical and chemical components, microorganisms, and pathological factors can exacerbate inflammation and organ damage. This review summarizes the induction and role of NETs in inflammation and focuses on the strategies of inhibiting NETosis and the mechanisms involved in pathogen evasion of NETs. Furthermore, herbal medicine inhibitors and nanodelivery strategies improve the efficiency of inhibition of excessive levels of NETs.

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“…This long-lasting DNase I improves the stability and half-life of the enzyme and inhibits NF-κB activation and cytokine levels, thereby suppressing neutrophil and NETs formation ( 246 ). 2C5 is a monoclonal antibody that is highly specific for intact nuclear histones and can target binding to NETs ( 247 ). Targeted nanocarriers of 2C5 and DNase I can target NETs and have clinical implications for the targeted removal of NETs ( 248 ).…”

Section: Treatment Of Dvt Via Netsmentioning

confidence: 99%

Neutrophil extracellular traps mediate deep vein thrombosis: from mechanism to therapy

Yao,

Ma,

et al. 2023

Front. Immunol.

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Deep venous thrombosis (DVT) is a part of venous thromboembolism (VTE) that clinically manifests as swelling and pain in the lower limbs. The most serious clinical complication of DVT is pulmonary embolism (PE), which has a high mortality rate. To date, its underlying mechanisms are not fully understood, and patients usually present with clinical symptoms only after the formation of the thrombus. Thus, it is essential to understand the underlying mechanisms of deep vein thrombosis for an early diagnosis and treatment of DVT. In recent years, many studies have concluded that Neutrophil Extracellular Traps (NETs) are closely associated with DVT. These are released by neutrophils and, in addition to trapping pathogens, can mediate the formation of deep vein thrombi, thereby blocking blood vessels and leading to the development of disease. Therefore, this paper describes the occurrence and development of NETs and discusses the mechanism of action of NETs on deep vein thrombosis. It aims to provide a direction for improved diagnosis and treatment of deep vein thrombosis in the near future.

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Monoclonal antibody 2C5 specifically targets neutrophil extracellular traps

Cited by 7 publications

References 55 publications

Autoantibodies in rheumatoid arthritis – rheumatoid factor, anticitrullinated protein antibodies and beyond

Autoantibodies in rheumatoid arthritis – rheumatoid factor, anticitrullinated protein antibodies and beyond

Role and Therapeutic Targeting Strategies of Neutrophil Extracellular Traps in Inflammation

Neutrophil extracellular traps mediate deep vein thrombosis: from mechanism to therapy

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