scholarly journals RB137 recognizes LL37 in neutrophil-extracellular trap-like (NET) structures in systemic lupus erythematosus and rheumatoid arthritis inflamed tissues by immunofluorescence in histological sections

2020 ◽  
Vol 3 (4) ◽  
pp. e235
Author(s):  
Roberto Lande ◽  
Stefano Alivernini ◽  
Barbara Tolusso ◽  
Francesca Spadaro ◽  
Mario Falchi ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Systemic Lupus Erythematosus ◽  
Lupus Erythematosus ◽  
Neutrophil Extracellular Trap ◽  
Human Tissues ◽  
Systemic Lupus ◽  
Native Form ◽  
Recombinant Monoclonal Antibody ◽  
Health And Disease ◽  
Extracellular Trap

Besides being a natural antibiotic, the human cathelicidin LL37, produced by epithelial cells and neutrophils, is an important immune-modulator. LL37 alone, or in complex with DNA, can activate inflammatory pathways in psoriasis, Systemic Lupus Erythematosus (SLE) and Rheumatoid Arthritis (RA). In this work, we describe the capacity of the recombinant monoclonal antibody RB137, previously shown to specifically recognize LL37 in its native form by ELISA, to detect LL37 by immunofluorescence in human tissues derived from SLE and RA patients. In these tissues, LL37 decorates DNA filaments resembling neutrophil-extracellular-trap (NET) structures. This antibody represents a valuable tool to detect the presence, the native state and the exact localization of LL37 in human tissues in health and disease.

scholarly journals Monoclonal antibodies RB139 and RB142 recognize citrullinated LL37 by immunofluorescence in histological sections in Systemic lupus erythematosus (SLE) and Rheumatoid arthritis (RA)

2020 ◽  
Vol 3 (4) ◽  
pp. e236
Author(s):  
Roberto Lande ◽  
Stefano Alivernini ◽  
Barbara Tolusso ◽  
Francesca Spadaro ◽  
Mario Falchi ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Systemic Lupus Erythematosus ◽  
Monoclonal Antibodies ◽  
Epithelial Cells ◽  
Lupus Erythematosus ◽  
Human Tissues ◽  
Systemic Lupus ◽  
Exact Localization ◽  
Health And Disease ◽  
Pleiotropic Functions

LL37 is a natural antibiotic, but is also a molecule with pleiotropic functions as well as an immune-modulator. LL37 is produced by epithelial cells and is present in neutrophils’ granules. LL37 alone, or in complex with DNA, can activate inflammatory pathways in psoriasis, systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). In this work, we describe the capacity of two recombinant monoclonal antibodies, RB139 and RB142, previously shown to specifically recognize LL37 in its citrullinated form (cit-LL37) by ELISA, to detect LL37 by immunofluorescence in human inflamed tissues derived from SLE and RA patients. Such antibodies represent previously unavailable tools to detect the presence, the citrullinated state and the exact localization of cit-LL37 in human tissues in health and disease.

scholarly journals Neutrophil extracellular trap release is associated with antinuclear antibodies in systemic lupus erythematosus and anti-phospholipid syndrome

Rheumatology ◽  
2018 ◽  
Vol 57 (7) ◽  
pp. 1228-1234 ◽  
Author(s):  
Maarten van der Linden ◽  
Lucas L van den Hoogen ◽  
Geertje H A Westerlaken ◽  
Ruth D E Fritsch-Stork ◽  
Joël A G van Roon ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Erythematosus ◽  
Antinuclear Antibodies ◽  
Neutrophil Extracellular Trap ◽  
Systemic Lupus ◽  
Extracellular Trap ◽  
Anti Phospholipid Syndrome

scholarly journals The impact of neutrophil extracellular trap from patients with systemic lupus erythematosus on the viability, CD11b expression and oxidative burst of healthy neutrophils

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Alimohammad Fatemi ◽  
Razieh Alipour ◽  
Hossein Khanahmad ◽  
Fereshteh Alsahebfosul ◽  
Alireza Andalib ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Erythematosus ◽  
Oxidative Burst ◽  
Neutrophil Extracellular Trap ◽  
Systemic Lupus ◽  
Cd11b Expression ◽  
Cell Mortality ◽  
Extracellular Trap ◽  
The Impact

Abstract Background NET (neutrophil extracellular trap) has been shown to directly influence inflammation; in SLE (systemic lupus erythematosus), it is reportedly a plausible cause for the broken self-tolerance that contributes to this pathology. Meanwhile, the role of NET is not easily explicable, and there is a serious discrepancy in the role of NET in SLE pathology and generally inflammation; in particular, the interactions of neutrophils with NET have been rarely inspected. This study evaluates the effect of NET on neutrophils in the context of SLE. The neutrophils were incubated by the collected NET (from SLE patients and healthy controls) and their expression of an activation marker, viability and oxidative burst ability were measured. Results The level of cell mortality, CD11b expression and the oxidative burst capacity were elevated in NET-treated neutrophils. Also, the elevation caused by the SLE NET was higher than that produced by the healthy NET. Conclusion The decreased neutrophil viability was not due to the increase in apoptosis; rather, it was because of the augmentation of other inflammatory cell-death modes. The upregulation of CD11b implies that NET causes neutrophils to more actively contribute to inflammation. The increased oxidative burst capacity of neutrophils can play a double role in inflammation. Overall, the effects induced by NET on neutrophils help prolong inflammation; accordingly, the NET collected from SLE patients is stronger than the NET from healthy individuals.

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