Blockade of interleukin-13-mediated cell activation by a novel inhibitory antibody to human IL-13 receptor α1

Krause, Sebastian; Behrends, Jochen; Borowski, Andreas; Lohrmann, Jens; Lang, Stefan; Myrtek, Daniel; Lorenzen, Thomas; Virchow, J. Christian; Luttmann, Werner; Friedrich, Karlheinz

doi:10.1016/j.molimm.2005.11.001

Cited by 22 publications

(10 citation statements)

References 34 publications

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“…This type of repeated airways exposure to allergen induces experimental asthma in mice that is dependent on the IL-4– and IL-13–activated signaling molecule STAT6 13. 15-LO-1 is an IL-4– and IL-13–induced product of airway epithelial cells,14 monocytes,15 and dendritic cells 16. The STAT6 pathway is important in this study, as suggested by the observation that STAT6-deficient mice did not demonstrate an allergen-induced expression of 12/15-LO transcripts in the lung (Fig 1, A ).…”

Section: Resultsmentioning

confidence: 99%

12/15-Lipoxygenase deficiency protects mice from allergic airways inflammation and increases secretory IgA levels

Hajek

Lindley

Favoreto

et al. 2008

Journal of Allergy and Clinical Immunology

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Section: Resultsmentioning

confidence: 99%

12/15-Lipoxygenase deficiency protects mice from allergic airways inflammation and increases secretory IgA levels

Hajek

Lindley

Favoreto

et al. 2008

Journal of Allergy and Clinical Immunology

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“…44 To acquire the "T2-Skewed" phenotype, we used a defined differentiation media supplemented with IL-13 to skew differentiation toward an in vitro model of chronic respiratory diseases, characterized by barrier dysfunction, 45 mucus production, 46 allergic responses, 46 and T2 responses. [47][48][49] Using this high-content in vitro model of the conducting airway, we characterized nominal and dosimetric dose-response relationships for AgNP-induced barrier dysfunction, GSH depletion, ROS production, lipid peroxidation, and cytotoxicity across genotypes, phenotypes, and exposures to understand G×P effects on AgNP toxicity. To our knowledge, this is the first study to use organotypic cultures as a high-content in vitro model of the conducting airway to characterize G×P effects on AgNP toxicity.…”

Section: Introductionmentioning

confidence: 99%

The Effects of Genotype × Phenotype Interactions on Silver Nanoparticle Toxicity in Organotypic Cultures of Murine Tracheal Epithelial Cells

Nicholas

Haick

Workman

et al. 2019

Preprint

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Silver nanoparticles (AgNP) are used in multiple applications but primarily in the manufacturing of antimicrobial products. Previous studies have identified AgNP toxicity in airway epithelial cells, but no in vitro studies to date have used organotypic cultures as a high-content in vitro model of the conducting airway to characterize the effects of interactions between host genetic and acquired factors, or gene × phenotype interactions (G×P), on AgNP toxicity. In the present study, we derived organotypic cultures from primary murine tracheal epithelial cells (MTEC) to characterize nominal and dosimetric dose-response relationships for AgNP-induced barrier dysfunction, glutathione (GSH) depletion, reactive oxygen species (ROS) production, lipid peroxidation, and cytotoxicity across two genotypes (A/J and C57BL/6J mice), two phenotypes ("Normal" and "Type 2[T2]-Skewed"), and two exposures (an acute exposure of 24 h and a subacute exposure of 4 hours, every other day, over 5 days [5×4 h]). We characterized the "T2-Skewed" phenotype as an in vitro model of chronic respiratory diseases, which was marked by increased sensitivity to AgNP-induced barrier dysfunction, GSH depletion, ROS production, lipid peroxidation, and cytotoxicity, suggesting that asthmatics are a sensitive population to AgNP exposures in occupational settings. This also suggests that exposure limits, which should be based upon the most sensitive population, should be derived using in vitro and in vivo models of chronic respiratory diseases. This study highlights the importance of considering dosimetry as well as G×P effects when screening and prioritizing potential respiratory toxicants. Such in vitro studies can be used to inform regulatory policy aimed at special protections for all populations.

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“…In this review, we have introduced a strategy for the development of anti‐cancer therapeutic mAb using rat cells expressing GFP‐fused oncoproteins as immunogens and rats as the immunized animal, since their antibody repertoire is superior to that of mice. This immunization protocol using cells transfected with cDNA coding target proteins will eventually be replaced by DNA immunization, ( 74–76 ) if lymphocytes sensitized to target proteins expressed in vivo for hybridoma formation can be efficiently collected from immunized animals. We successfully obtained various mAb recognizing the extracellular domain of type I (human and mouse CD44v and CD44s, and four human HER family proteins), type II (TfR and CD98hc) and type IV (human LAT1, y+LAT2, ASC1, xCT, and human and mouse S1P1) membrane proteins.…”

Section: Conclusion With Additional Discussionmentioning

confidence: 99%

Towards therapeutic antibodies to membrane oncoproteins by a robust strategy using rats immunized with transfectants expressing target molecules fused to green fluorescent protein

et al. 2010

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Cell‐surface molecules containing growth factor receptors, adhesion molecules and transporter proteins are often over‐expressed in various cancer cells, and could be regarded as suitable targets for therapeutic monoclonal antibodies (mAb). Anti‐cancer therapeutic mAb are claimed to bind these cell‐surface molecules on viable cancer cells: therefore, it is necessary to produce mAb recognizing epitopes on the extracellular domains of native but not denatured proteins. We have experienced difficulty in obtaining mAb bound to viable cancer cells using synthetic peptides or recombinant proteins produced in bacteria as immunogens, although these immunogens are relatively easy to prepare. In this context, we have concluded that viable cancer cells or cells transfected with cDNA encoding target proteins are suitable immunogens for the production of anti‐cancer therapeutic mAb. Furthermore, we selected rats as the immunized animals, because of their excellent capacity to generate diverse antibodies. Because many target candidates are multi‐pass (type IV) membrane proteins, such as 7‐pass G protein‐coupled receptors and 12‐pass transporter proteins belonging to the solute carrier family, and their possible immunogenic extracellular regions are very small, production of specific mAb was extremely difficult. In this review, we summarize the successful preparation and characterization of rat mAb immunized against the extracellular domain of type I, type II and type IV membrane oncoproteins fused to green fluorescent protein as an approach using reverse genetics, and also introduce the discovery of cell‐death‐inducing antibodies as an approach using forward genetics and a strategy to produce reshaped antibodies using mimotope peptides as the immunogen. (Cancer Sci 2011; 102: 25–35)

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Blockade of interleukin-13-mediated cell activation by a novel inhibitory antibody to human IL-13 receptor α1

Cited by 22 publications

References 34 publications

12/15-Lipoxygenase deficiency protects mice from allergic airways inflammation and increases secretory IgA levels

12/15-Lipoxygenase deficiency protects mice from allergic airways inflammation and increases secretory IgA levels

The Effects of Genotype × Phenotype Interactions on Silver Nanoparticle Toxicity in Organotypic Cultures of Murine Tracheal Epithelial Cells

Towards therapeutic antibodies to membrane oncoproteins by a robust strategy using rats immunized with transfectants expressing target molecules fused to green fluorescent protein

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