Adoptively transferred late allergic response is inhibited by IL-4, but not IL-5, antisense oligonucleotide Sophie Molet, PhD, David Ramos-Barbón, MD,

Slides:

Advertisements

Similar presentations

Dual effects of vitamin D–induced alteration of TH1/TH2 cytokine expression Victor Matheu, MD, Ove Bäck, MD, PhD, Emma Mondoc, BSc, Shohreh Issazadeh-Navikas,

Advertisements

Gene expression of vascular endothelial growth factor and its receptors and angiogenesis in bronchial asthma Makoto Hoshino, MDa, Yutaka Nakamura, MDa,

Russell S. Traister, MD, PhD, Crystal E. Uvalle, BS, Gregory A

Diesel exhaust particulate induces airway hyperresponsiveness in a murine model: Essential role of GM-CSF Ken Ohta, MD, PhD, Naomi Yamashita, MD, PhD,

Heat-killed Lactobacillus plantarum L-137 suppresses naturally fed antigen–specific IgE production by stimulation of IL-12 production in mice Shinji.

IL-4 induces IL-13–independent allergic airway inflammation

Effective prevention and therapy of experimental allergic asthma using a GATA-3– specific DNAzyme Serdar Sel, MD, Michael Wegmann, PhD, Tanja Dicke, MSc,

CD4 T-helper cells engineered to produce IL-10 prevent allergen-induced airway hyperreactivity and inflammation Jae-Won Oh, MD, PhD, Christine M. Seroogy,

Allergy prevention starts before conception: Maternofetal transfer of tolerance protects against the development of asthma Tobias Polte, PhD, Christian.

Local administration of antisense phosphorothioate oligonucleotides to the c-kit ligand, stem cell factor, suppresses airway inflammation and IL-4 production.

Frank Kirstein, PhD, Natalie E

Compartmentalized chemokine-dependent regulatory T-cell inhibition of allergic pulmonary inflammation Roshi Afshar, PhD, James P. Strassner, BS, Edward.

Role of IL-9 in the pathophysiology of allergic diseases

Leukocyte nicotinamide adenine dinucleotide phosphate-reduced oxidase is required for isocyanate-induced lung inflammation Si-Yen Liu, PhD, Wei-Zhi Wang,

CD4+ T cells migrate from airway to bone marrow after antigen inhalation in rats Susumu Isogai, MD, Shigeru Miyata, MD, Rame Taha, MD, Yasuyuki Yoshizawa,

Eosinophils contribute to the resolution of lung-allergic responses following repeated allergen challenge Katsuyuki Takeda, MD, PhD, Yoshiki Shiraishi,

Grass pollen immunotherapy inhibits allergen-induced infiltration of CD4+ T lymphocytes and eosinophils in the nasal mucosa and increases the number of.

T lymphocytes in asthma: Bronchial versus peripheral responses

Surfactant protein D inhibits TNF-α production by macrophages and dendritic cells in mice László Hortobágyi, MS, Sonja Kierstein, PhD, Kateryna Krytska,

Frank Kirstein, PhD, Natalie E

Inhibition of house dust mite–induced allergic airways disease by antagonism of microRNA-145 is comparable to glucocorticoid treatment Adam Collison,

Requirements for allergen-induced airway inflammation and hyperreactivity in CD4- deficient and CD4-sufficient HLA-DQ transgenic mice Svetlana P. Chapoval,

Susan C. Foley, MD, David Préfontaine, MSc, Qutayba Hamid, MD, PhD

Dendritic cells modulated by cytokine-expressing adenoviruses alleviate eosinophilia and airway hyperresponsiveness in an animal model of asthma Yi-Ling.

Prostaglandin E2 suppresses allergic sensitization and lung inflammation by targeting the E prostanoid 2 receptor on T cells Zbigniew Zasłona, PhD, Katsuhide.

Regulation of allergic airway inflammation by class I–restricted allergen presentation and CD8 T-cell infiltration James W. Wells, PhD, Christopher J.

Jesús Merayo-Lloves, MD, Tong Z. Zhao, MD, James E. Dutt, BA, C

Zoulfia Allakhverdi, PhD, Michael R. Comeau, BSc, Dirk E

Prostaglandin E2 suppresses allergic sensitization and lung inflammation by targeting the E prostanoid 2 receptor on T cells Zbigniew Zasłona, PhD, Katsuhide.

Role of B cells in TH cell responses in a mouse model of asthma

Downregulation of a disintegrin and metalloproteinase 33 by IFN-γ in human airway smooth muscle cells Isao Ito, MD, PhD, Johanne D. Laporte, PhD, Pierre.

Sarita Sehra, PhD, Weiguo Yao, PhD, Evelyn T. Nguyen, MS, Nicole L

Evidence for expression of eosinophil-associated IL-12 messenger RNA and immunoreactivity in bronchial asthma Esra Nutku, MDa, Abdelilah Soussi Gounni,

Pathophysiology of the inflammatory response

Basophils and eosinophils in allergic rhinitis

Inflammatory cells, cytokine and chemokine expression in asthma immunocytochemistry and in situ hybridization Qutayba Hamid, MD, PhD, Editor Journal.

Recruitment of T cells to the lung in response to antigen challenge

Increased IL-33 expression by epithelial cells in bronchial asthma

The leukocyte activation antigen CD69 limits allergic asthma and skin contact hypersensitivity Pilar Martín, PhD, Manuel Gómez, PhD, Amalia Lamana, PhD,

Volume 119, Issue 1, Pages (July 2000)

Kirthana Ganeshan, BS, Colleen V

IFN-τ inhibits IgE production in a murine model of allergy and in an IgE-producing human myeloma cell line Mustafa G. Mujtaba, PhDa, Lorelie Villarete,

IL-12 affects Dermatophagoides farinae–induced IL-4 production by T cells from pediatric patients with mite-sensitive asthma Takeshi Noma, MD, PhD, Izumi.

Eosinophilia and gastrointestinal symptoms after ingestion of shiitake mushrooms Aaron M. Levy, MDa, Hirohito Kita, MDb, Sidney F. Phillips, MDa, Paul.

IL-9 expression by human eosinophils: Regulation by IL-1β and TNF-α

Corticosteroid-induced apoptosis in mouse airway epithelium: Effect in normal airways and after allergen-induced airway inflammation Delbert R. Dorscheid,

Enhanced production of CCL18 by tolerogenic dendritic cells is associated with inhibition of allergic airway reactivity Iris Bellinghausen, PhD, Sebastian.

Differential regulation of cytokine expression after allergen exposure of sensitized rats by cyclosporin A and corticosteroids: Relationship to bronchial.

Mast cells regulate IFN-γ expression in the skin and circulating IgE levels in allergen- induced skin inflammation Harri Alenius, PhD, Dhafer Laouini,

IL-10–treated dendritic cells decrease airway hyperresponsiveness and airway inflammation in mice Toshiyuki Koya, MD, PhD, Hiroyuki Matsuda, MD, PhD,

TH1/TH2 cytokines and inflammatory cells in skin biopsy specimens from patients with chronic idiopathic urticaria: Comparison with the allergen-induced.

Antibody to very late activation antigen 4 prevents interleukin-5–induced airway hyperresponsiveness and eosinophil infiltration in the airways of guinea.

Harald Renz, MD, Chaya Brodie, PhD, Katherine Bradley, BS, Donald Y. M

Molecular pathology of allergic disease

Ligation of IgE receptors causes an anaphylactic response and neutrophil infiltration but does not induce eosinophilic inflammation in mice Masayuki.

Rhinovirus infection interferes with induction of tolerance to aeroantigens through OX40 ligand, thymic stromal lymphopoietin, and IL-33 Amit K. Mehta,

No defect in T-cell priming, secondary response, or tolerance induction in response to inhaled antigens in Fms-like tyrosine kinase 3 ligand–deficient.

IL-13 induces eosinophil recruitment into the lung by an IL-5– and eotaxin-dependent mechanism Samuel M. Pope, BAa,b, Eric B. Brandt, PhDa, Anil Mishra,

DNA methylation of TH1/TH2 cytokine genes affects sensitization and progress of experimental asthma Stephanie Brand, PhD, Dörthe Andrea Kesper, PhD,

CCL17/thymus and activation-regulated chemokine induces calcitonin gene–related peptide in human airway epithelial cells through CCR4 Kandace Bonner,

Inhibition of allergic airways inflammation and airway hyperresponsiveness in mice by dexamethasone: Role of eosinophils, IL-5, eotaxin, and IL-13 Seok-Yong.

Suplatast tosilate inhibits goblet-cell metaplasia of airway epithelium in sensitized mice Jae Jeong Shim, MD, Karim Dabbagh, PhD, Kiyoshi Takeyama, MD,

Monocyte chemotactic proteins in allergen-induced inflammation in the nasal mucosa: Effect of topical corticosteroids Pota Christodoulopoulos, BSca,

Local expression of ϵ germline gene transcripts and RNA for the ϵ heavy chain of IgE in the bronchial mucosa in atopic and nonatopic asthma Sun Ying,

Abnormalities of cell and mediator levels in bronchoalveolar lavage fluid of patients with mild asthma Sally E. Wenzel, MD Journal of Allergy and Clinical.

Cytokine profile in minor salivary glands from patients with bronchial asthma Anne Tsicopoulos, MDa, b, Anne Janin, MDc, Hikmat Akoum, PhDa, Catherine.

IL-4– and IL-5–positive T lymphocytes, eosinophils, and mast cells in allergen-induced late-phase cutaneous reactions in atopic subjects Luis T. Barata,

The extra domain A of fibronectin is essential for allergen-induced airway fibrosis and hyperresponsiveness in mice Martin Kohan, MSc, Andres F. Muro,

Local treatment with IL-12 is an effective inhibitor of airway hyperresponsiveness and lung eosinophilia after airway challenge in sensitized mice Jürgen.

CCL17/thymus and activation-regulated chemokine induces calcitonin gene–related peptide in human airway epithelial cells through CCR4 Kandace Bonner,

Presentation transcript:

Adoptively transferred late allergic response is inhibited by IL-4, but not IL-5, antisense oligonucleotide Sophie Molet, PhD, David Ramos-Barbón, MD, James G. Martin, MD, Qutayba Hamid, MD, PhD Journal of Allergy and Clinical Immunology Volume 104, Issue 1, Pages 205-214 (July 1999) DOI: 10.1016/S0091-6749(99)70137-5 Copyright © 1999 Mosby, Inc. Terms and Conditions

Fig. 1 Schematic diagram representing one example of the mechanism by which AS ODNs work. AS ODNs act on the translation stage. Usually designed to hybridize specifically to a particular sequence of mRNA, AS ODNs block the access of mRNA to the ribosomes, thus preventing translation in the protein of interest. Then mRNA degradation is promoted by an RNase H-dependent agent (RNase H specifically degrades the RNA strand of RNA/DNA hybrid). Consequently, the production of a targeted protein is inhibited. Journal of Allergy and Clinical Immunology 1999 104, 205-214DOI: (10.1016/S0091-6749(99)70137-5) Copyright © 1999 Mosby, Inc. Terms and Conditions

Fig. 2 Time course of R L after OVA challenge in BN rats. Unsensitized animals were injected intraperitoneally with CD4 + T cells treated with culture medium (controls [Co] , n = 9, open circles ) or NP-Y AS (irrelevant AS, filled circles , n = 13), IL-5 AS ( filled squares , n = 8), or IL-4 AS ( open triangles , n = 9) ODNs. Two days later, the animals were challenged with a 5% OVA aerosol. R L was measured every 5 minutes during a 20-minute period and subsequently every 15 minutes over a period of 8 hours. Journal of Allergy and Clinical Immunology 1999 104, 205-214DOI: (10.1016/S0091-6749(99)70137-5) Copyright © 1999 Mosby, Inc. Terms and Conditions

Fig. 3 Airway response to OVA in BN rats. Unsensitized animals were injected intraperitoneally with CD4 + T cells treated with culture medium (controls [Co] , n = 9, hatched bar ) or NP-Y AS (irrelevant AS, open bar , n = 13), IL-5 AS ( shaded bar , n = 8), or IL-4 AS ( filled bar , n = 9) ODNs. Two days later, the animals were challenged with a 5% OVA aerosol. R L was measured for 8 hours and analyzed during the first hour for the development of an EAR (A) and from 1 to 3 hours (B) and 3 to 8 hours for the measurement of the LAR (C) . EAR was quantified by taking the maximal value of R L during the first 60 minutes after OVA challenge above the baseline (results expressed as percentage of baseline). LAR was calculated as the area under the R L versus time curve above the baseline values from 3 to 8 hours (results expressed as AUC). Results are expressed as means ± SEM. Probability (P) values were determined by using the nonparametric Kruskal-Wallis test. Journal of Allergy and Clinical Immunology 1999 104, 205-214DOI: (10.1016/S0091-6749(99)70137-5) Copyright © 1999 Mosby, Inc. Terms and Conditions

Fig. 4 Representative photomicrographs of BAL cells recovered from control rats ( A and C ) and from rats that received IL-4 AS–treated CD4 + T cells ( B and D ). Specific staining shown is for MBP-positive eosinophils ( A and B ; black arrows ) and IL-4–immunoreactive cells ( C and D ; white arrows ). Journal of Allergy and Clinical Immunology 1999 104, 205-214DOI: (10.1016/S0091-6749(99)70137-5) Copyright © 1999 Mosby, Inc. Terms and Conditions

Fig. 5 Eosinophilia in BAL fluid investigated by immunocytochemistry. BAL fluid was recovered at the end of the experiment (8 hours after OVA challenge) from the recipients of culture medium (controls [Co], n = 9, circles) or NP-Y AS– (irrelevant AS, triangles, n = 8), IL-5 AS– (squares, n = 8), or IL-4 AS– (diamonds, n = 8) treated CD4+ T cells. Eosinophils were detected by the APAAP method by using the BMK-13 antibody, a mouse anti-human MBP mAb. Results are expressed as the number of MBP+ cells per 103 BAL cells counted for each rat. Probability (P) values were determined by using ANOVA, and the Fisher test was applied to test for differences. Journal of Allergy and Clinical Immunology 1999 104, 205-214DOI: (10.1016/S0091-6749(99)70137-5) Copyright © 1999 Mosby, Inc. Terms and Conditions

Fig. 6 IL-4 expression in BAL fluid investigated by immunocytochemistry. BAL fluid was recovered at the end of the experiment (8 hours after OVA challenge) from the recipients of culture medium (controls [Co], n = 9, circles) or NP-Y AS– (irrelevant AS, triangles, n = 8), IL-5 AS– (squares, n = 8) or IL-4 AS– (diamonds, n = 8) treated CD4+ T cells. IL-4 was detected by the streptavidin/biotin–alkaline phosphatase conjugated method by using a biotinylated goat anti-mouse IL-4 antibody. Results are expressed as the number of IL-4+ cells per 103 BAL cells counted for each rat. Probability (P) values were determined by using ANOVA, and the Fisher test was applied to test for differences. Journal of Allergy and Clinical Immunology 1999 104, 205-214DOI: (10.1016/S0091-6749(99)70137-5) Copyright © 1999 Mosby, Inc. Terms and Conditions

Fig. 7 IL-5 expression in BAL fluid investigated by immunocytochemistry. BAL fluid was recovered at the end of the experiment (8 hours after OVA challenge) from the recipients of culture medium (controls [Co] , n = 9, circles ) or NP-Y AS– (irrelevant AS, triangles , n = 7), IL-5 AS– ( squares , n = 8) or IL-4 AS– ( diamonds , n = 8) treated CD4 + T cells. IL-5 was detected by the APAAP method by using a mouse anti-rat IL-5 mAb. Results are expressed as the number of IL-5 + cells per 10 3 BAL cells counted for each rat. Probability (P) values were determined by using ANOVA, and the Fisher test was applied to test for differences. Journal of Allergy and Clinical Immunology 1999 104, 205-214DOI: (10.1016/S0091-6749(99)70137-5) Copyright © 1999 Mosby, Inc. Terms and Conditions

Fig. 8 IFN-γ expression in BAL fluid investigated by immunocytochemistry. BAL fluid was recovered at the end of the experiment (8 hours after OVA challenge) from the recipients of culture medium (controls [Co], n = 9, circles) or NP-Y AS– (irrelevant AS, triangles, n = 7), IL-5 AS– (squares, n = 8), or IL-4 AS– (diamonds, n = 8) treated CD4+ T cells. IFN-γ was detected by the APAAP method by using a mouse anti-rat IFN-γ mAb. Results are expressed as the number of IFN-γ+ cells per 103 BAL cells counted for each rat. Probability (P) values were determined by using ANOVA, and the Fisher test was applied to test for differences. Journal of Allergy and Clinical Immunology 1999 104, 205-214DOI: (10.1016/S0091-6749(99)70137-5) Copyright © 1999 Mosby, Inc. Terms and Conditions