LAUREN E COHN

Summary

Affiliation: Yale University
Country: USA

Publications

  1. ncbi request reprint IL-4-independent induction of airway hyperresponsiveness by Th2, but not Th1, cells
    L Cohn
    Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520 8011, USA
    J Immunol 161:3813-6. 1998
  2. pmc T helper 1 cells and interferon gamma regulate allergic airway inflammation and mucus production
    L Cohn
    Section of Pulmonary Medicine, Yale University School of Medicine, New Haven, Connecticut 06520, USA
    J Exp Med 190:1309-18. 1999
  3. ncbi request reprint T-helper type 2 cell-directed therapy for asthma
    L Cohn
    Section of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Yale University School of Medicine, 333 Cedar Street, PO Box 208057, 06520 8057, New Haven, CT, USA
    Pharmacol Ther 88:187-96. 2000
  4. ncbi request reprint IL-4 promotes airway eosinophilia by suppressing IFN-gamma production: defining a novel role for IFN-gamma in the regulation of allergic airway inflammation
    L Cohn
    Sections of Pulmonary and Critical Care Medicine and Immunobiology, Department of Dermatology and Department of Pathology, Yale University School of Medicine, New Haven, CT 06520, USA
    J Immunol 166:2760-7. 2001
  5. ncbi request reprint Asthma: mechanisms of disease persistence and progression
    Lauren Cohn
    Yale University School of Medicine, Section of Pulmonary and Critical Care Medicine, New Haven, Connecticut, USA
    Annu Rev Immunol 22:789-815. 2004
  6. pmc Mucus in chronic airway diseases: sorting out the sticky details
    Lauren Cohn
    Section of Pulmonary and Critical Care Medicine, Yale University School of Medicine, New Haven, Connecticut 06520 8057, USA
    J Clin Invest 116:306-8. 2006
  7. pmc Advances in mucous cell metaplasia: a plug for mucus as a therapeutic focus in chronic airway disease
    David R Curran
    Section of Pulmonary and Critical Care, Yale University School of Medicine, New Haven, CT 06520, USA
    Am J Respir Cell Mol Biol 42:268-75. 2010

Research Grants

Collaborators

Detail Information

Publications7

  1. ncbi request reprint IL-4-independent induction of airway hyperresponsiveness by Th2, but not Th1, cells
    L Cohn
    Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520 8011, USA
    J Immunol 161:3813-6. 1998
    ..Thus, IL-4 production by Th2 cells is not essential for the induction of AHR, but is critical for the migration of eosinophils from lung tissue into the airways...
  2. pmc T helper 1 cells and interferon gamma regulate allergic airway inflammation and mucus production
    L Cohn
    Section of Pulmonary Medicine, Yale University School of Medicine, New Haven, Connecticut 06520, USA
    J Exp Med 190:1309-18. 1999
    ..The blockade of eosinophilia and mucus production by IFN-gamma likely occurs through different inhibitory pathways that are activated downstream of Th2 cytokine secretion and require IFN-gamma signaling in tissue of recipient mice...
  3. ncbi request reprint T-helper type 2 cell-directed therapy for asthma
    L Cohn
    Section of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Yale University School of Medicine, 333 Cedar Street, PO Box 208057, 06520 8057, New Haven, CT, USA
    Pharmacol Ther 88:187-96. 2000
    ..Furthermore, we explore newer immunomodulatory strategies to inhibit Th2 cell effects, including therapies that may block Th2 cell differentiation, neutralize cytokines, and redirect immune responses towards Th1 and away from Th2...
  4. ncbi request reprint IL-4 promotes airway eosinophilia by suppressing IFN-gamma production: defining a novel role for IFN-gamma in the regulation of allergic airway inflammation
    L Cohn
    Sections of Pulmonary and Critical Care Medicine and Immunobiology, Department of Dermatology and Department of Pathology, Yale University School of Medicine, New Haven, CT 06520, USA
    J Immunol 166:2760-7. 2001
    ..We define a new regulatory role for IFN-gamma, demonstrating that eosinophilic inflammation is differentially regulated at distinct sites within the respiratory tract...
  5. ncbi request reprint Asthma: mechanisms of disease persistence and progression
    Lauren Cohn
    Yale University School of Medicine, Section of Pulmonary and Critical Care Medicine, New Haven, Connecticut, USA
    Annu Rev Immunol 22:789-815. 2004
    ..We review human and animal data detailing the cellular and molecular interactions in established allergic asthma that promote persistent disease, amplify inflammation, and, in turn, cause disease progression...
  6. pmc Mucus in chronic airway diseases: sorting out the sticky details
    Lauren Cohn
    Section of Pulmonary and Critical Care Medicine, Yale University School of Medicine, New Haven, Connecticut 06520 8057, USA
    J Clin Invest 116:306-8. 2006
    ..This begs the question, Is it possible to reduce airway obstruction in chronic lung disease by inhibiting EGFR activation and/or by inhibiting IL-13?..
  7. pmc Advances in mucous cell metaplasia: a plug for mucus as a therapeutic focus in chronic airway disease
    David R Curran
    Section of Pulmonary and Critical Care, Yale University School of Medicine, New Haven, CT 06520, USA
    Am J Respir Cell Mol Biol 42:268-75. 2010
    ..We now have a greater incentive to focus on inhibition of mucus as a therapy for chronic airway diseases...

Research Grants11

  1. T CELL CONTROL OF AIRWAY MUCUS PRODUCTION
    Lauren Cohn; Fiscal Year: 2003
    ..abstract_text> ..
  2. T CELL CONTROL OF AIRWAY MUCUS PRODUCTION
    Lauren Cohn; Fiscal Year: 2009
    ..AIM II. Determine the mechanism of IFN-g inhibition of eosinophilia and its relationship to the reciprocal induction of neutrophilia. AIM III. Determine how IFN-g regulates the number of Th2 cells in the respiratory tract. ..
  3. Airway Inflammation-Related Inhibition of Disease (AIRID)
    LAUREN E COHN; Fiscal Year: 2010
    ..We will define the cells and factors that are responsible for the protective effect and determine if this pathway can be activated to treat chronic lung diseases, such as asthma and sarcoidosis. ..