IL-13 induces airways hyperreactivity independently of the IL-4rα chain in the allergic lung

Journal of Immunology

Volumn 167, Issue 3, 2001, Pages 1683-1692

  Mattes, J ^a   Yang, M ^a   Siqueira, A ^a   Clark, K ^a   MacKenzie, J ^a   McKenzie, A N J ^a   Webb, D C ^a   Matthaei, K I ^a   Foster, P S ^a  

^a AUSTRALIAN NATIONAL UNIVERSITY   (Australia)

Author keywords

[No Author keywords available]

Indexed keywords

CYTOKINE; EOTAXIN; INTERLEUKIN 13; INTERLEUKIN 13 RECEPTOR; INTERLEUKIN 13 RECEPTOR ALPHA1; INTERLEUKIN 4 RECEPTOR; INTERLEUKIN 4 RECEPTOR ALPHA; OVALBUMIN; STAT6 PROTEIN; UNCLASSIFIED DRUG;

AIRWAY OBSTRUCTION; ANIMAL CELL; ARTICLE; ASTHMA; BRONCHUS HYPERREACTIVITY; CONTROLLED STUDY; EOSINOPHILIA; LYMPHOCYTE ACTIVATION; MOUSE; NONHUMAN; PATHOGENESIS; PRIORITY JOURNAL; T LYMPHOCYTE;

EID: 0035424185     PISSN: 00221767     EISSN: None     Source Type: Journal    
DOI: 10.4049/jimmunol.167.3.1683     Document Type: Article

References (67)

1. Immunological basis of antigen-induced airways hyperresponsiveness
2. Asthma and inflammation
3. Immunological aspects of allergic asthma
4. Asthma: A dynamic disease of inflammation and repair
5. The relationship between airway inflammation and bronchial hyperresponsiveness
6. Relation between airway responsiveness and serum IgE in children with asthma and in apparently normal children
7. Allergic and nonallergic asthmatics have distinct patterns of T-cell activation and cytokine production in peripheral blood and bronchoalveolar lavage
8. Predominant TH2-like bronchoalveolar T-lymphocyte population in atopic asthma
9. + T cells, increased TH2-type cytokine mRNA expression, and eosinophil recruitment in bronchoalveolar lavage after allergen inhalation challenge in patients with atopic asthma
10. + T-lymphocytes and interleukin-5 mediate antigen-induced eosinophil infiltration into the mouse trachea
11. + T lymphocytes prevents antigen-induced airway hyperreactivity and pulmonary eosinophilia
12. A novel T cell-regulated mechanism modulating allergen-induced airways hyperreactivity in BALB/c mice independently of IL-4 and IL-5
13. Eosinophil recruitment to the lung in a murine model of allergic inflammation: The role of T cells, chemokines, and adhesion receptors
14. Successful transfer of late phase eosinophil infiltration in the lung by infusion of helper T cell clones
15. Induction of airway mucus production by T helper 2 (Th2) cells: A critical role for interleukin 4 in cell recruitment but not mucus production
16. Aeroallergen-induced eosinophilic inflammation, lung damage, and airways hyperreactivity in mice can occur independently of IL-4 and allergen-specific immunoglobulins
17. Cooperation between Th1 and Th2 cells in a murine model of eosinophilic airway inflammation
18. Effects of Th2 cytokines on chemokine expression in the lung: IL-13 potently induces eotaxin expression by airway epithelial cells
19. Interleukin-4-dependent pulmonary eosinophil infiltration in a murine model of asthma
20. Interleukin 5 deficiency abolishes eosinophilia, airways hyperreactivity, and lung damage in a mouse asthma model
21. Interleukin 4, but not interleukin 5 or eosinophils, is required in a murine model of acute airway hyperreactivity
22. + T cell IL-4 production is revealed in IL-4 receptor-deficient mice
23. Interleukin-5 and eosinophils induce airway damage and bronchial hyperreactivity during allergic airway inflammation in BALB/c mice
24. Antiinterleukin-5 antibody prevents airway hyperresponsiveness in a murine model of airway sensitization
25. Interleukin-5 expression in the lung epithelium of transgenic mice leads to pulmonary changes pathognomonic of asthma
26. Interleukin-13: Central mediator of allergic asthma
27. Interleukin-9 promotes allergen-induced eosinophilic inflammation and airway hyperresponsiveness in transgenic mice
28. Requirement for IL-13 independently of IL-4 in experimental asthma
29. Th2-induced airway mucus production is dependent on IL-4Rα, but not on eosinophils
30. IL-4-independent induction of airway hyperresponsiveness by Th2, but not Th1, cells
31. Pulmonary expression of interleukin-13 causes inflammation, mucus hypersecretion, subepithelial fibrosis, physiologic abnormalities, and eotaxin production
32. IL-10 is necessary for the expression of airway hyperresponsiveness but not pulmonary inflammation after allergic sensitization
33. CC chemokine receptor (CCR)3/eotaxin is followed by CCR4/monocyte-derived chemokine in mediating pulmonary T helper lymphocyte type 2 recruitment after serial antigen challenge in vivo
34. Allergen-induced airway inflammation and bronchial responsiveness in wild-type and interleukin-4-deficient mice
35. Interleukin-4 receptor blockade prevents airway responses induced by antigen challenge in mice
36. Interleukin 13, a T-cell-derived cytokine that regulates human monocyte and B-cell function
37. Activated mast cells produce interleukin 13
38. Production of interleukin 13 by alveolar macrophages from normal and fibrotic lung
39. Interleukin-13, an interleukin-4 like cytokine that acts on monocytes and B cells, but not on T cells
40. Receptors for interleukin-13 and interleukin-4 are complex and share a novel component that functions in signal transduction
41. The role of shared receptor motifs and common Stat proteins in the generation of cytokine pleiotropy and redundancy by IL-2, IL-4, IL-7, IL-13, and IL-15
42. Abrogation of bronchial eosinophilic inflammation and airway hyperreactivity in signal transducers and activators of transcription (STAT)6-deficient mice
43. Signal transducer and activator of transcription factor 6 (Stat6)-deficient mice are protected from antigen-induced airway hyperresponsiveness and mucus production
44. The failure of STAT6-deficient mice to develop airway eosinophilia and airway hyperresponsiveness is overcome by interleukin-5
45. STAT6: An intracellular target for the inhibition of allergic disease
46. A soluble form of IL-13 receptor α1 promotes IgG2a and IgG2b production by murine germinal center B cells
47. Impaired development of Th2 cells in IL-13-deficient mice
48. Essential role of Stat6 in IL-4 signalling
49. + T cells play a pivotal role in aeroallergen-induced eosinophilia, bronchial hyperreactivity, and lung damage in mice
50. Fluorescent dyes for lymphocyte migration and proliferation studies
51. Integrated signals between IL-13, IL-4, and IL-5 regulate airways hyperreactivity
52. Noninvasive measurement of airway responsiveness in allergic mice using barometric plethysmography
53. A general method for the construction of recombinant vaccinia viruses expressing multiple foreign genes
54. The effect of IL-5 and eotaxin expression in the lung on eosinophil trafficking and degranulation and the induction of bronchial hyperreactivity
55. Activation of eotaxin gene transcription by NF-κB and STAT6 in human airway epithelial cells
56. Genetic variants of IL-13 signalling and human asthma and atopy
57. IL-13 expression at the sites of allergen challenge in patients with asthma
58. Interleukin-13 and interleukin-4 are coexpressed in atopic asthma
59. Allergen-specific Th1 cells fail to counterbalance Th2 cell-induced airway hyperreactivity but cause severe airway inflammation
60. Cytokine production by T cell clones from bronchoalveolar lavage fluid of patients with asthma and healthy subjects
61. Relationship between interleukin-5 and eotaxin in regulating blood and tissue eosinophilia in mice
62. T cell-dependent regulation of eotaxin in antigen-induced pulmonary eosinophilia
63. Th2-induced eotaxin expression and eosinophilia coexist with Th1 responses at the effector stage of lung inflammation
64. 4 integrin-dependent eotaxin induction of bronchial hyperresponsiveness and eosinophil migration in interleukin-5 transgenic mice
65. Eotaxin induces a rapid release of eosinophils and their progenitors from the bone marrow
66. Cloning and characterization of a binding subunit of the interleukin 13 receptor that is also a component of the interleukin 4 receptor
67. Aluminum hydroxide adjuvant initiates strong antigen-specific Th2 responses in the absence of IL-4- or IL-13-mediated signaling