Normal and viral-infected rainbow trout (RT) were tested for serum antibody activity against self and nonself antigens. Particularly high titres of anti-trinitrophenyl (TNP) antibodies were noted, as in other fish species. To analyse this, the anti-TNP antibodies were isolated by affinity chromatography and their capacity to interfere with viral infection in vitro was studied. We selected RT fibroblasts as target cells, and two common pathogenic viruses in trout, a rhabdovirus, viral haemorrhagic septicaemia virus (VHS) and a birnavirus, the infectious pancreatic necrosis virus (IPN). Anti-TNP antibodies were examined for their capacity to neutralize VHS and IPN viruses. Data obtained show that the anti-TNP antibodies, even at high concentrations, only partially neutralized virus. In contrast, when anti-TNP antibodies were assayed for their protective activity using RT fibroblast cells infected with VHS or IPN viruses, results showed high protective activity, regardless of serum origin or of the virus used, when the antibodies were added to the cell culture after viral infection. Therefore, our experiments indicate that the protective activity does not seem to be due to a direct interaction of the antibodies with the viruses. It is suggested that virus-modified cell surface self structures exhibit new epitopes which interact with the anti-TNP antibodies. Such an interaction would allow anti-TNP antibodies to participate in a non-specific defence mechanism against viral infection.
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http://dx.doi.org/10.1016/0923-2494(89)90021-7 | DOI Listing |
Front Immunol
November 2024
Department of Basic and Translational Sciences, School of Dental Medicine, University of Pennsylvania, Philadelphia, PA, United States.
Introduction: Allergic asthma has been linked to the activation of mast cells (MCs) by the neuropeptide substance P (SP), but the mechanism underlying this neuroimmune interaction is unknown. Substance P produced from cutaneous nociceptors activates MCs via Mas-related G-protein-coupled receptor B2 (MrgprB2) to enhance type 2 immune response in experimental atopic dermatitis in mice. We recently showed that the adapter protein β-arrestin2 (β-arr2) contributes to MrgprB2-mediated MC chemotaxis.
View Article and Find Full Text PDFPediatr Rheumatol Online J
May 2023
Immunology Laboratory, Immunology Department, Hellenic Pasteur Institute, 127, Vasilissis Sofias Avenue, 11521, Athens, Greece.
Protein Pept Lett
January 2021
Biomedical Innovations Research for Translational Health Science (BIRTHS) Laboratory, Department of Biochemistry and Molecular Biology, College of Medicine, University of the Philippines, Manila, Philippines
Background: Microbe-Binding Peptides (MBPs) are currently being investigated to address the problem of antimicrobial resistance. Strategies enhancing their antimicrobial activity have been developed, including peptide dimerization. Here, we present an alternative approach based on peptide polymerization, yielding hapten-labelled polymeric MBPs that mediate tagging of bacteria with anti-hapten antibodies, for enhanced immune recognition by host phagocytes.
View Article and Find Full Text PDFToxicol Pathol
June 2020
Global Discovery & Development Sciences, Novo Nordisk A/S, Måløv, Denmark.
Administration of human protein-based drugs to animals often leads to formation of antidrug antibodies (ADAs) that may form circulating immune complexes (CICs) with the dosed protein. Circulating immune complexes can activate and bind complement (cCICs), and if large amount of CICs or cCICs is formed, the clearance mechanism potentially becomes saturated, which can lead to immune complex (IC) deposition and inflammation. To obtain a better understanding of the underlying factors, including the relationship between different dose regimes on IC formation and deposition and identification of possible biomarkers of IC deposition and IC-related pathological changes in kidneys, BALB/c and C57BL/6J mice were administered with human anti-tumor necrosis factor α (aTNFα, adalimumab) or a humanized anti-TNP (aTNP) antibody for 13 weeks.
View Article and Find Full Text PDFArthritis Rheumatol
September 2020
IDIVAL and Instituto de Biomedicina y Biotecnología de Cantabria, CSIC-Universidad de Cantabria-SODERCAN, Santander, Spain.
Objective: The transforming growth factor β (TGFβ) inhibitor BAMBI (bone morphogenetic protein and activin membrane-bound inhibitor) has been shown to control differentiation of CD4+ T lymphocytes into either tolerogenic Treg cells or pathogenic Th17 cells, through the regulation of TGFβ and interleukin-2 (IL-2) signaling strength. The present study was undertaken to explore the potential beneficial effects of this strategy of pharmacologic inhibition using novel anti-BAMBI monoclonal antibodies (mAb) in different experimental murine models of chronic skin and joint inflammatory/autoimmune disease.
Methods: Development of Saccharomyces cerevisiae mannan-induced psoriatic arthritis (MIP) (n = 18-30 mice per group), imiquimod-induced skin psoriasis (n = 20-30 mice per group), or type II collagen-induced arthritis (CIA) (n = 13-16 mice per group) was analyzed in a total of 2-5 different experiments with either wild-type (WT) or BAMBI-deficient B10.
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