L Cohn

Summary

Affiliation: Yale University
Country: USA

Publications

  1. pmc Induction of airway mucus production By T helper 2 (Th2) cells: a critical role for interleukin 4 in cell recruitment but not mucus production
    L Cohn
    Section of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520, USA
    J Exp Med 186:1737-47. 1997
  2. 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
  3. ncbi request reprint Inhibition of allergic inflammation in a murine model of asthma by expression of a dominant-negative mutant of GATA-3
    D H Zhang
    Department of Medicine, Yale University School of Medicine, New Haven, Connecticut 06520, USA
    Immunity 11:473-82. 1999
  4. 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
  5. ncbi request reprint Th2-induced airway mucus production is dependent on IL-4Ralpha, but not on eosinophils
    L Cohn
    Sections of Pulmonary and Critical Care Medicine and Immunobiology and Department of Pathology, Yale University School of Medicine, New Haven, CT 06520, USA
    J Immunol 162:6178-83. 1999
  6. ncbi request reprint A critical role for NF-kappa B in GATA3 expression and TH2 differentiation in allergic airway inflammation
    J Das
    Department of Medicine, Pulmonary and Critical Care Section, Yale University School of Medicine, 333 Cedar Street, LCI 105, New Haven, CT 06520, USA
    Nat Immunol 2:45-50. 2001
  7. 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
  8. 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
  9. pmc Essential role of nuclear factor kappaB in the induction of eosinophilia in allergic airway inflammation
    L Yang
    Department of Internal Medicine, Pulmonary and Critical Care Section, Yale University School of Medicine, New Haven, Connecticut 06520, USA
    J Exp Med 188:1739-50. 1998
  10. ncbi request reprint Altering the Th1/Th2 balance as a therapeutic strategy in asthmatic diseases
    A Ray
    Department of Internal Medicine, Yale University School of Medicine, 333 Cedar Street, 105 LCI, New Haven, CT 06520 8057, USA
    Curr Opin Investig Drugs 1:442-8. 2000

Collaborators

Detail Information

Publications10

  1. pmc Induction of airway mucus production By T helper 2 (Th2) cells: a critical role for interleukin 4 in cell recruitment but not mucus production
    L Cohn
    Section of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520, USA
    J Exp Med 186:1737-47. 1997
    ..These data suggest that IL-4 is crucial for Th2 cell recruitment to the lung and for induction of inflammation, but has no direct role in mucus production...
  2. 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...
  3. ncbi request reprint Inhibition of allergic inflammation in a murine model of asthma by expression of a dominant-negative mutant of GATA-3
    D H Zhang
    Department of Medicine, Yale University School of Medicine, New Haven, Connecticut 06520, USA
    Immunity 11:473-82. 1999
    ..Thus, targeting GATA-3 activity alone is sufficient to blunt Th2 responses in vivo, thereby establishing GATA-3 as a potential therapeutic target in the treatment of asthma and allergic diseases...
  4. 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...
  5. ncbi request reprint Th2-induced airway mucus production is dependent on IL-4Ralpha, but not on eosinophils
    L Cohn
    Sections of Pulmonary and Critical Care Medicine and Immunobiology and Department of Pathology, Yale University School of Medicine, New Haven, CT 06520, USA
    J Immunol 162:6178-83. 1999
    ..These studies show definitively that IL-5, eosinophils, or mast cells are not essential, but signaling through IL-4Ralpha is critically important in Th2 cell stimulation of mucus production...
  6. ncbi request reprint A critical role for NF-kappa B in GATA3 expression and TH2 differentiation in allergic airway inflammation
    J Das
    Department of Medicine, Pulmonary and Critical Care Section, Yale University School of Medicine, 333 Cedar Street, LCI 105, New Haven, CT 06520, USA
    Nat Immunol 2:45-50. 2001
    ..Our studies provide a molecular basis for the need for both T cell receptor and cytokine signaling for GATA-3 expression and, in turn, TH2 differentiation...
  7. 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...
  8. 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...
  9. pmc Essential role of nuclear factor kappaB in the induction of eosinophilia in allergic airway inflammation
    L Yang
    Department of Internal Medicine, Pulmonary and Critical Care Section, Yale University School of Medicine, New Haven, Connecticut 06520, USA
    J Exp Med 188:1739-50. 1998
    ..These results demonstrate a crucial role for NF-kappaB in vivo in the expression of important molecules that have been implicated in the pathogenesis of asthma...
  10. ncbi request reprint Altering the Th1/Th2 balance as a therapeutic strategy in asthmatic diseases
    A Ray
    Department of Internal Medicine, Yale University School of Medicine, 333 Cedar Street, 105 LCI, New Haven, CT 06520 8057, USA
    Curr Opin Investig Drugs 1:442-8. 2000
    ..In the clinical trial arena, the unmet challenging goal remains to convert the concept of Th1/Th2 balance modulation, without deleterious side effects, into clinical practice for the management of asthmatic disease...