Intranasal treatment with a recombinant hypoallergenic derivative of the major birch pollen allergen Bet v 1 prevents allergic sensitization and airway inflammation in mice

International Archives of Allergy and Immunology

Volumn 126, Issue 1, 2001, Pages 68-77

  Wiedermann, Ursula ^a   Herz, Udo ^b   Baier, Karin ^a   Vrtala, Susanne ^a   Neuhaus Steinmetz, Ulrich ^b   Bohle, Barbara ^a   Dekan, Gerhard ^a   Renz, Harald ^b   Ebner, Christof ^a   Valenta, Rudolf ^a   Kraft, Dietrich ^a  

^a UNIVERSITY OF VIENNA   (Austria)

^b UNIVERSITY HOSPITAL MARBURG   (Germany)

Author keywords

Animal model, in vivo; BALB c; Bet v 1; Birch pollen; Mucosa; Recombinant hypoallergenic fragments; Tolerance suppression; Type I allergy

Indexed keywords

ANTIALLERGIC AGENT; EPITOPE; GAMMA INTERFERON; IMMUNOGLOBULIN E ANTIBODY; IMMUNOGLOBULIN G ANTIBODY; IMMUNOGLOBULIN G1 ANTIBODY; INTERLEUKIN 10; INTERLEUKIN 5; MESSENGER RNA; POLLEN ANTIGEN; RECOMBINANT ANTIGEN; TRANSFORMING GROWTH FACTOR BETA; UNCLASSIFIED DRUG;

AEROSOL; ALLERGIC ASTHMA; ALLERGIC REACTION; ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ANTIBODY PRODUCTION; ANTIBODY RESPONSE; ARTICLE; CELL STIMULATION; CELL TRANSFER; CONFORMATION; CONTROLLED STUDY; CYTOKINE PRODUCTION; EOSINOPHILIA; FEMALE; GENE EXPRESSION; GENETIC ENGINEERING; IMMEDIATE TYPE HYPERSENSITIVITY; IMMUNE RESPONSE; IMMUNOLOGICAL TOLERANCE; IMMUNOMODULATION; LYMPHOCYTE PROLIFERATION; MOUSE; NONHUMAN; NOSE MUCOSA; PLANT; PRIORITY JOURNAL; PROPHYLAXIS; RESPIRATORY TRACT ALLERGY; RESPIRATORY TRACT INFLAMMATION; SENSITIZATION; SKIN ALLERGY; SPLEEN CELL; T LYMPHOCYTE;

ADMINISTRATION, INTRANASAL; ADOPTIVE TRANSFER; ALLERGENS; ANIMALS; BETULA; CYTOKINES; DESENSITIZATION, IMMUNOLOGIC; FEMALE; HYPERSENSITIVITY, IMMEDIATE; IMMUNE TOLERANCE; IMMUNITY, MUCOSAL; IMMUNOGLOBULIN E; IMMUNOGLOBULIN G; LUNG; MICE; MICE, INBRED BALB C; PLANT PROTEINS; POLLEN; RECOMBINANT PROTEINS; RNA, MESSENGER; T-LYMPHOCYTES; TRANSFORMING GROWTH FACTOR BETA;

EID: 17944365808     PISSN: 10182438     EISSN: None     Source Type: Journal    
DOI: 10.1159/000049496     Document Type: Article

References (40)

1. Isolation and characterization of the major allergen of birch pollen (Betula verrucosa)
2. IgE and IgG antibodies of patients with allergy to birch pollen as tools to define the allergen profile of Betula verrucosa
3. Recombinant allergens for immunoblot diagnosis of tree pollen allergy
4. The gene coding for the major birch pollen allergen, Bet v 1, is highly homologous to a pea disease resistance response gene
5. Identification of multiple T cell epitopes on Bet v 1, the major birch pollen allergen, using specific T cell clones and overlapping peptides
6. Purification and characterization of recombinant Bet v 1, the major birch pollen allergen
7. Dissection of immunoglobulin E and T cell reactivity of isoforms of the major birch pollen allergen Bet v1: Potential use of hypoallergenic isoforms for immunotherapy
8. Conversion of the major birch pollen allergen, Bet v 1, into two nonanaphylactic T cell epitope-containing fragments: Candidates for a novel form of specific immunotherapy
9. Modulation of IgE reactivity of allergens by site-directed mutagenesis: Potential use of hypoallergenic variants for immunotherapy
10. Comparison of genetically engineered hypoallergenic rBet v 1 derivatives with rBet v 1 wild-type by skin prick and intradermal testing: Results obtained in a French population
11. The influence of exposure to house dust mite, cat, pollen and fungal allergens in the home to primary sensitization in asthma
12. Breast feeding as prophylaxis against atopic disease: A prospective follow-up study until 17 years old
13. Grass pollen immunotherapy inhibits allergen induced infiltration of CD4+ T lymphocytes and eosinophils in the basal mucosa and increases in the number of cells expressing messenger RNA for interferon-gamma
14. Immunological changes during specific immunotherapy of grass pollen allergy: Reduced lymphoproliferative responses to allergen and shift from Th2 to Th1 in T cell clones specific for Phl p 1, a major grass pollen allergen
15. Oral tolerance in disease
16. Peptide-induced T cell regulation of experimental autoimmune encephalomyelitis: A role for IL-10
17. Mechanisms of nasal tolerance induction in experimental autoimmune myasthenia gravis: Identification of regulatory cells
18. Regulation of IgE responses to inhaled antigen in mice by antigen-specific γδ T cells
19. Aerosol-induced immunoglobulin(Ig)-E unresponsiveness to ovalbumin does not require CD8+ or T cell receptor (TCR)-γ/δ T cells or interferon (IFN)-γ in a murine model of allergen sensitization
20. Suppression of antigen-specific T and B cell responses by intranasal or oral administration of recombinant Bet v 1, the major birch pollen allergen, in a murine model of type I allergy
21. Suppressive versus stimulatory effects of allergen/cholera toxoid (CTB) conjugates depending on the nature of the allergen in a murine model of type I allergy
22. Modulation of the allergic immune response in BALB/c mice by subcutaneous injection of high doses of the dominant epitope from the major birch pollen allergen Bet v 1
23. Oligodeoxynucleotides containing CpG motifs modulate the allergic immune response of BALB/c mice to Bet v 1, the major birch pollen allergen
24. Sequential development of airway hyperresponsiveness and acute airway obstruction in a mouse model of allergic inflammation
25. Characterization of the specificity and duration of T cell tolerance to intranasally administered peptides in mice: A role of intramolecular epitope suppression
26. Inducing tolerance by intranasal administration of long peptides in naive and primed CBA/J mice
27. The epidemic of allergy and asthma
28. Eosinophil recruitment into the respiratory epithelium following antigenic challenge in hyper-IgE mice is accompanied by interleukin 5-dependent bronchial hyperresponsiveness
29. Interleukin 4, but not interleukin 5 or eosinophils, is required in a murine model of acute airway hyperreactivity
30. Development of eosinophilic airway inflammation and airway hyperresponsiveness requires interleukin-5 but not immunoglobulin E or B lymphocytes
31. Mechanisms preventing allergen-induced airway hyperreactivity: Role of tolerance and immune deviation
32. A novel T cell regulated mechanism modulating allergen-induced airway hyperreactivity in BALB/c mice independently of IL-4 and IL-5
33. Differential regulation of T cell cytokine pattern and IgE and IgG4 responses by conformational epitopes
34. Oral tolerance, an active immunological process mediated by multiple mechanisms
35. Oral administration of an immunodominant T cell epitope downregulates Th1/Th2 cytokines and prevents experimental myasthenia gravis
36. CD4+ T helper cells engineered to produce latent TGF-β1 reverse allergen-induced airway hyperreactivity and inflammation
37. A CD4+ T cell subset inhibits antigen-specific T cell responses and prevents colitis
38. Regulatory Th2-type T cell lines against insulin and GAD peptides derived from orally and nasally treated NOD mice suppress diabetes
39. The natural immune response to inhaled soluble protein antigens involves major histocompatibility complex (MHC) class I restricted CD8+ T cell mediated but MHC class II restricted CD4+ T cell dependent immune deviation resulting in selective suppression of immunoglobulin E production
40. Effects of CD8+ T cell depletion on bronchial hyper-responsiveness and inflammation in sensitized and allergen-exposed Brown-Nor-way rats