IL-13 is associated with reduced illness and replication in primary respiratory syncytial virus infection in the mouse

[1]  R. Peebles,et al.  Differential immune responses and pulmonary pathophysiology are induced by two different strains of respiratory syncytial virus. , 2006, The American journal of pathology.

[2]  S. Weiss,et al.  Endosomal Proteolysis by Cathepsins Is Necessary for Murine Coronavirus Mouse Hepatitis Virus Type 2 Spike-Mediated Entry , 2006, Journal of Virology.

[3]  B. Turk,et al.  Cysteine cathepsins in the immune response. , 2006, Tissue antigens.

[4]  Nikolaos M. Nikolaidis,et al.  Persistent effects induced by IL-13 in the lung. , 2006, American journal of respiratory cell and molecular biology.

[5]  Kathryn L. Schornberg,et al.  Role of Endosomal Cathepsins in Entry Mediated by the Ebola Virus Glycoprotein , 2006, Journal of Virology.

[6]  J. Crowe,et al.  Identification of an H-2Db-restricted CD8+ cytotoxic T lymphocyte epitope in the matrix protein of respiratory syncytial virus , 2005 .

[7]  J. Whitsett,et al.  Surfactant protein-d enhances phagocytosis and pulmonary clearance of respiratory syncytial virus. , 2004, American journal of respiratory cell and molecular biology.

[8]  E. Gelfand,et al.  Respiratory syncytial virus-induced airway hyperresponsiveness is independent of IL-13 compared with that induced by allergen. , 2003, The Journal of allergy and clinical immunology.

[9]  J. Berzofsky,et al.  Transforming Growth Factor-β Production and Myeloid Cells Are an Effector Mechanism through Which CD1d-restricted T Cells Block Cytotoxic T Lymphocyte–mediated Tumor Immunosurveillance , 2003, The Journal of Experimental Medicine.

[10]  T. Wynn.  IL-13 effector functions. , 2003, Annual review of immunology.

[11]  R. Parker,et al.  IL-13 Is Sufficient for Respiratory Syncytial Virus G Glycoprotein-Induced Eosinophilia After Respiratory Syncytial Virus Challenge 1 , 2003, The Journal of Immunology.

[12]  J. Berzofsky,et al.  A push–pull approach to maximize vaccine efficacy: Abrogating suppression with an IL-13 inhibitor while augmenting help with granulocyte/macrophage colony-stimulating factor and CD40L , 2002, Proceedings of the National Academy of Sciences of the United States of America.

[13]  B. Ma,et al.  Overlapping and enzyme-specific contributions of matrix metalloproteinases-9 and -12 in IL-13-induced inflammation and remodeling. , 2002, The Journal of clinical investigation.

[14]  B. Ma,et al.  Pulmonary type II cell hypertrophy and pulmonary lipoproteinosis are features of chronic IL-13 exposure. , 2002, American journal of physiology. Lung cellular and molecular physiology.

[15]  B. Graham,et al.  The Role of IFN in Respiratory Syncytial Virus Pathogenesis , 2002, The Journal of Immunology.

[16]  C. Hogaboam,et al.  Respiratory Syncytial Virus Predisposes Mice to Augmented Allergic Airway Responses Via IL-13-Mediated Mechanisms1 , 2001, The Journal of Immunology.

[17]  H. Maassab,et al.  IL-13-Induced Airway Hyperreactivity During Respiratory Syncytial Virus Infection Is STAT6 Dependent1 , 2001, The Journal of Immunology.

[18]  R. Parker,et al.  Respiratory syncytial virus infection does not increase allergen‐induced type 2 cytokine production, yet increases airway hyperresponsiveness in mice , 2001, Journal of medical virology.

[19]  B. Ma,et al.  Inducible targeting of IL-13 to the adult lung causes matrix metalloproteinase- and cathepsin-dependent emphysema. , 2000, The Journal of clinical investigation.

[20]  L. Montaner,et al.  IL‐13 and TNF‐α  inhibit dual‐tropic HIV‐1 in primary macrophages by reduction of surface expression of CD4, chemokine receptors CCR5, CXCR4 and post‐entry viral gene expression , 2000 .

[21]  B. Graham,et al.  IL-4 Diminishes Perforin-Mediated and Increases Fas Ligand-Mediated Cytotoxicity In Vivo1 , 2000, The Journal of Immunology.

[22]  B. Graham,et al.  Interleukin-4 Diminishes CD8+ Respiratory Syncytial Virus-Specific Cytotoxic T-Lymphocyte Activity In Vivo , 1999, Journal of Virology.

[23]  B. Graham,et al.  Secreted Respiratory Syncytial Virus G Glycoprotein Induces Interleukin-5 (IL-5), IL-13, and Eosinophilia by an IL-4-Independent Mechanism , 1999, Journal of Virology.

[24]  J. Whitsett,et al.  Surfactant protein-A enhances respiratory syncytial virus clearance in vivo. , 1999, The Journal of clinical investigation.

[25]  D D Donaldson,et al.  Interleukin-13: central mediator of allergic asthma , 1998 .

[26]  D D Donaldson,et al.  The murine IL-13 receptor alpha 2: molecular cloning, characterization, and comparison with murine IL-13 receptor alpha 1. , 1998, Journal of immunology.

[27]  G. McKenzie,et al.  Impaired development of Th2 cells in IL-13-deficient mice. , 1998, Immunity.

[28]  F. Brombacher,et al.  Differences between IL-4Rα-deficient and IL-4-deficient mice reveal a role for IL-13 in the regulation of Th2 responses , 1998, Current Biology.

[29]  B. Graham,et al.  Priming with Secreted Glycoprotein G of Respiratory Syncytial Virus (RSV) Augments Interleukin-5 Production and Tissue Eosinophilia after RSV Challenge , 1998, Journal of Virology.

[30]  F. Finkelman,et al.  IL-13, IL-4Ralpha, and Stat6 are required for the expulsion of the gastrointestinal nematode parasite Nippostrongylus brasiliensis. , 1998, Immunity.

[31]  B. Graham,et al.  Overexpression of interleukin-4 delays virus clearance in mice infected with respiratory syncytial virus , 1997, Journal of virology.

[32]  L. Montaner,et al.  IL‐13 acts on macrophages to block the completion of reverse transcription, inhibit virus production, and reduce virus infectivity , 1997, Journal of leukocyte biology.

[33]  J. Groopman,et al.  Differential effects of interleukin-13 on cytomegalovirus and human immunodeficiency virus infection in human alveolar macrophages. , 1997, Blood.

[34]  M. Rolph,et al.  Interleukin-4 mediates down regulation of antiviral cytokine expression and cytotoxic T-lymphocyte responses and exacerbates vaccinia virus infection in vivo , 1996, Journal of virology.

[35]  J. G. Zhang,et al.  Cloning and characterization of a binding subunit of the interleukin 13 receptor that is also a component of the interleukin 4 receptor. , 1996, Proceedings of the National Academy of Sciences of the United States of America.

[36]  M. Denis,et al.  Interleukin 13 and interleukin 4 protect bronchoalveolar macrophages from productive infection with human immunodeficiency virus type 1. , 1994, AIDS research and human retroviruses.

[37]  L. Montaner,et al.  Interleukin 13 inhibits human immunodeficiency virus type 1 production in primary blood-derived human macrophages in vitro , 1993, The Journal of experimental medicine.

[38]  P. Openshaw,et al.  Pulmonary eosinophilic response to respiratory syncytial virus infection in mice sensitized to the major surface glycoprotein G. , 1992, International immunology.

[39]  M. Perkins,et al.  Primary respiratory syncytial virus infection in mice , 1988, Journal of medical virology.

[40]  J. Crowe,et al.  Identification of an H-2D(b)-restricted CD8+ cytotoxic T lymphocyte epitope in the matrix protein of respiratory syncytial virus. , 2005, Virology.

[41]  B. Graham,et al.  The complex relationship between respiratory syncytial virus and allergy in lung disease. , 2003, Viral immunology.

[42]  Y. Kook,et al.  Respiratory syncytial virus infection induces matrix metalloproteinase-9 expression in epithelial cells , 2002, Archives of Virology.

[43]  J. D. de Vries,et al.  Interleukin 13, an interleukin 4-like cytokine that acts on monocytes and B cells, but not on T cells. , 1994, Immunology today.