Cutting edge: IL-4-independent induction of airway hyperresponsiveness by Th2, but not Th1, cells

L Cohn, JS Tepper, K Bottomly - The Journal of Immunology, 1998 - journals.aai.org
L Cohn, JS Tepper, K Bottomly
The Journal of Immunology, 1998journals.aai.org
We investigated the role of Th1 or Th2 cells in airway hyperresponsiveness (AHR), because
both IFN-γ 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 …
Abstract
We investigated the role of Th1 or Th2 cells in airway hyperresponsiveness (AHR), because both IFN-γ 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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