ArticleClinical and experimental immunology1995
A systematic study of neutrophil degranulation and respiratory burst in vitro by defined immune complexes.
Article in Clinical and experimental immunology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 46 citations in OpenAlex.
- Trial
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- Selenium Nanoparticles Can Influence the Immune Response Due to Interactions with Antibodies and Modulation of the Physiological State of Granulocytes.Pharmaceutics · 2022Article
- Granulocyte colony-stimulating factor as a cause of acute leucocytoclastic vasculitis with anti-Ro and anti-La antibodies.BMJ case reports · 2022Article
- Genetic Background Affects the Mucosal Secretory IgA Levels, Parasite Burden, Lung Inflammation, and Mouse Susceptibility toInfection and immunity · 2022Article
- Platelets and IgE: Shaping the Innate Immune Response in Systemic Lupus Erythematosus.Clinical reviews in allergy & immunology · 2020Review
- Heterogeneity in neutrophil responses to immune complexes.Blood advances · 2019Article
- Neutrophil oxidative burst as a diagnostic indicator of IgG-mediated anaphylaxis.Blood research · 2018Article
- Effect of CXCR2 Inhibition on Behavioral Outcomes and Pathology in Rat Model of Neuromyelitis Optica.Journal of immunology research · 2018Article
- Honokiol suppresses formyl peptide-induced human neutrophil activation by blocking formyl peptide receptor 1.Scientific reports · 2017Article
- Matrix metalloproteinases as input and output signals for post-myocardial infarction remodeling.Journal of molecular and cellular cardiology · 2016Review
- Posttranslational Modifications and the Immunogenicity of Biotherapeutics.Journal of immunology research · 2016Review
- Immunogenicity of antibody drug conjugates: bioanalytical methods and monitoring strategy for a novel therapeutic modality.The AAPS journal · 2015Article
- Assessment of the neutrophilic antibody-dependent respiratory burst (ADRB) response to Plasmodium falciparum.Journal of leukocyte biology · 2014Article
- A white paper--consensus and recommendations of a global harmonization team on assessing the impact of immunogenicity on pharmacokinetic measurements.The AAPS journal · 2014Review
- Regulation of innate immune response to Candida albicans infections by αMβ2-Pra1p interaction.Infection and immunity · 2011Article
- Inhibition of erythrocyte invasion and Plasmodium falciparum merozoite surface protein 1 processing by human immunoglobulin G1 (IgG1) and IgG3 antibodies.Infection and immunity · 2009Article
- Antibodies against a surface protein of Streptococcus pyogenes promote a pathological inflammatory response.PLoS pathogens · 2008Article
- Neutrophil lactoferrin release induced by IgA immune complexes differed from that induced by cross-linking of fcalpha receptors (FcalphaR) with a monoclonal antibody, MIP8a.Clinical and experimental immunology · 2000Article
- Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Defined immune complexes (IC) were used to compare the effect of antibodies of different classes and subclasses on neutrophil respiratory burst and degranulation. IC were made from 5-iodo-4-hydroxy-3-nitrophenacetyl (NIP) conjugated to bovine serum albumin (BSA) and chimaeric mouse-human anti-NIP monoclonal antibodies including IgA2, IgE and all four IgG subclasses. The activation of neutrophils by IC depended on antibody class and subclass, on antigen epitope density, on antigen: antibody ratio and on the medium used. The ability to generate the respiratory burst showed a different pattern to the ability to give rise to degranulation. Compared with other IC, IgA2 IC provided the strongest stimulus for neutrophil activation. IgG1 IC, IgG2 IC and IgG4 IC activated neutrophils moderately or weakly IgG3 IC were unable to stimulate the respiratory burst, but could cause strong degranulation. IgE IC could hardly cause any neutrophil response. Neutrophil degranulation in response to IgG3 IC in serum-free medium or heat-inactivated serum was fast, and it quickly reached maximum. Degranulation caused by IgA IC was relatively slow, but gradually increased during incubation. The activity of IgG1 IC, IgG2 IC and IgG4 IC generated a respiratory burst increased with antibody excess and decreased with antigen excess. The activity of IgA2 IC, however, was not affected by change of antigen and antibody ratio. A specific role of serum, possibly due to complement, was found in enhancing degranulation, both temporally and quantitatively, by IgA2 IC.
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