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CUTTING EDGE |


Sections of
*
Immunobiology and
Pulmonary and Critical Care Medicine, Yale University School of Medicine, New Haven, CT 06520;
Immunology Research, Genentech, Inc., South San Francisco, CA 94080; and
§
Howard Hughes Medical Institute, New Haven, CT 06536
We investigated the role of Th1 or Th2 cells in airway
hyperresponsiveness (AHR), because both IFN-
and IL-4 and
IL-5-producing CD4 T cells have been identified in the airways of
asthmatics. After transfer of in vitro-generated TCR transgenic Th1 or
Th2 cells and exposure to inhaled Ag, Th2 cells induced AHR and airway
eosinophilia, whereas Th1 cells induced neutrophilic
inflammation without AHR. Next, to determine the precise effector
function of IL-4 in Th2 cell-induced AHR, we transferred
IL-4-/- Th2 cells into wild-type and
IL-4-/- recipient mice. After exposure to inhaled Ag,
both groups of mice exhibited AHR with markedly reduced airway
eosinophilia. 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.
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J. Wang, R. J. Homer, L. Hong, L. Cohn, C. G. Lee, S. Jung, and J. A. Elias IL-11 Selectively Inhibits Aeroallergen-Induced Pulmonary Eosinophilia and Th2 Cytokine Production J. Immunol., August 15, 2000; 165(4): 2222 - 2231. [Abstract] [Full Text] [PDF] |
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L. H. Glimcher and K. M. Murphy Lineage commitment in the immune system: the T helper lymphocyte grows up Genes & Dev., July 15, 2000; 14(14): 1693 - 1711. [Full Text] |
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D. C. Webb, A. N. J. McKenzie, A. M. L. Koskinen, M. Yang, J. Mattes, and P. S. Foster Integrated Signals Between IL-13, IL-4, and IL-5 Regulate Airways Hyperreactivity J. Immunol., July 1, 2000; 165(1): 108 - 113. [Abstract] [Full Text] [PDF] |
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H. Matsuse, A. K. Behera, M. Kumar, H. Rabb, R. F. Lockey, and S. S. Mohapatra Recurrent Respiratory Syncytial Virus Infections in Allergen-Sensitized Mice Lead to Persistent Airway Inflammation and Hyperresponsiveness J. Immunol., June 15, 2000; 164(12): 6583 - 6592. [Abstract] [Full Text] [PDF] |
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N. M. Munoz, G. A. van Seventer, R. T. Semnani, and A. R. Leff Augmentation of LTC4 synthesis in human eosinophils caused by CD3-stimulated Th2-like cells in vitro Am J Physiol Lung Cell Mol Physiol, June 1, 2000; 278(6): L1172 - L1179. [Abstract] [Full Text] [PDF] |
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M. Castro, D. D. Chaplin, M. J. Walter, and M. J. Holtzman Could Asthma Be Worsened by Stimulating the T-helper Type 1 Immune Response? Am. J. Respir. Cell Mol. Biol., February 1, 2000; 22(2): 143 - 146. [Full Text] |
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W. R. Henderson Jr., E. Y. Chi, and C. R. Maliszewski Soluble IL-4 Receptor Inhibits Airway Inflammation Following Allergen Challenge in a Mouse Model of Asthma J. Immunol., January 15, 2000; 164(2): 1086 - 1095. [Abstract] [Full Text] [PDF] |
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L. Cohn, R. J. Homer, N. Niu, and K. Bottomly T Helper 1 Cells and Interferon {gamma} Regulate Allergic Airway Inflammation and Mucus Production J. Exp. Med., November 1, 1999; 190(9): 1309 - 1318. [Abstract] [Full Text] [PDF] |
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M. A. Aronica, A. L. Mora, D. B. Mitchell, P. W. Finn, J. E. Johnson, J. R. Sheller, and M. R. Boothby Preferential Role for NF-{kappa}B/Rel Signaling in the Type 1 But Not Type 2 T Cell-Dependent Immune Response In Vivo J. Immunol., November 1, 1999; 163(9): 5116 - 5124. [Abstract] [Full Text] [PDF] |
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L. Cohn, R. J. Homer, H. MacLeod, M. Mohrs, F. Brombacher, and K. Bottomly Th2-Induced Airway Mucus Production Is Dependent on IL-4R{alpha}, But Not on Eosinophils J. Immunol., May 15, 1999; 162(10): 6178 - 6183. [Abstract] [Full Text] [PDF] |
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I.-C. HO, J.I. KIM, S.J. SZABO, and L.H. GLIMCHER Tissue-specific Regulation of Cytokine Gene Expression Cold Spring Harb Symp Quant Biol, January 1, 1999; 64(0): 573 - 584. [Abstract] [PDF] |
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