Results 111 to 120 of about 19,431 (234)

NETosis in Autoimmune Diseases

open access: yesJournal of Rheumatic Diseases, 2016
Neutrophils are the major antimicrobial cells of the innate immune system, which are recruited rapidly to the sites of infection and provide the primary defense against pathogens. Recent evidence suggests that neutrophils undergo a distinct cell death mechanism called NETosis, which not only contributes to the host defense, but also leads to severe ...
openaire   +1 more source

Genetic Susceptibility to Periodontitis

open access: yesJournal of Periodontal Research, EarlyView.
Aim: The aim of this narrative review was to identify genes carrying risk alleles associated with an increased risk of periodontitis and to place them in a biological context. Methods: The literature was reviewed based on predefined criteria. Results: The identified genes largely fall into functions linking immune response with tissue repair. The genes
Gesa M. Richter, Arne S. Schaefer
wiley   +1 more source

Platelet-derived HMGB1 induces NETosis, exacerbating brain damage in the photothrombotic stroke model

open access: yesMolecular Medicine
Following cerebral ischemia, neutrophil extracellular traps (NETs) contribute significantly to brain damage by exacerbating delayed immune cell infiltration and vascular injury. They are detected both in brain tissue and within blood vessels.
Sang-A. Oh   +4 more
doaj   +1 more source

From patients with arthralgia, pre-RA and recently diagnosed RA: What is the current status of understanding RA pathogenesis? [PDF]

open access: yes, 2018
It is believed that therapy for rheumatoid arthritis (RA) is the most effective and beneficial within a short time frame around RA diagnosis. This insight has caused a shift from research in patients with established RA to patients at risk of developing ...
Hazes, J.M.W. (Mieke)   +2 more
core   +1 more source

Inflammatory and Immunological Basis of Periodontal Diseases

open access: yesJournal of Periodontal Research, EarlyView.
The periodontal lesion emerges as an evolving immunological battlefield, where host–microbiome interactions, dysregulated immune responses, fragile resolution mechanisms, and inflammophilic dysbiosis converge to shift the balance from homeostasis to unrestrained tissue destruction.
Giacomo Baima   +3 more
wiley   +1 more source

Apoptotic Vesicles Attenuate Acute Lung Injury via CD73-Mediated Inhibition of Platelet Activation and NETosis

open access: yesInternational Journal of Nanomedicine
Lingping Tan,1,2,* Chi Zhang,1,2,* Xiaoxing Kou,1– 3 Lu Zhao,4 Di Wu,1– 3 Jinyu Li,1,2 Chuanying Yu,1,2 Tansi Xu,1,2 Li Gao,1,2 Xueli Mao,1– 3 Chuanjiang Zhao1,2 1Hospital of Stomatology, Guanghua School of Stomatology, Sun Yat-sen University ...
Tan L   +10 more
doaj  

Autoimmunity and Periodontitis

open access: yesJournal of Periodontal Research, EarlyView.
In a microbe‐driven inflammatory environment, peptidyl‐arginine deiminase (PAD) enzymes from neutrophils and Porphyromonas gingivalis citrullinate both microbial and self‐antigens. B cell presentation of citrullinated or self‐mimicking epitopes activates T cells that assist B cells in antibody isotype switching, affinity maturation, epitope spreading ...
Massimo Costalonga   +2 more
wiley   +1 more source

Case Report: Anti-platelet factor 4 -mediated immunothrombosis in a patient with ANCA vasculitis – a shared mechanism of NETosis

open access: yesFrontiers in Immunology
Anti-platelet factor 4 (PF4) immunothrombosis is characterized by thrombocytopenia, thrombosis and enhanced NETosis and has been described in the absence of prior heparin exposure.
Lital Remez-Gabay   +8 more
doaj   +1 more source

Sepsis Induces a Dysregulated Neutrophil Phenotype That Is Associated with Increased Mortality

open access: yesMediators of Inflammation, 2018
Background. Neutrophil dysfunction in sepsis has been implicated in the pathogenesis of multiorgan failure; however, the role of neutrophil extracellular traps (NETs) remains uncertain.
Jaimin M. Patel   +6 more
doaj   +1 more source

Home - About - Disclaimer - Privacy