Antigen-stimulated lung CD4+ cells produce IL-5, while lymph node CD4+ cells produce Th2 cytokines concomitant with airway eosinophilia and hyperresponsiveness

Autor: Hofstra, C. L., Ark, I. Van, Kool, M., Nijkamp, F. P., Oosterhout, A. J. M. Van
Zdroj: Inflammation Research; 19991101, Vol. 48 Issue: 11 p602-612, 11p
Abstrakt: Abstract. Objective and Design: We investigated whether airway inflammation in a mouse model of allergic asthma is related to antigen-specific T cell responses in the effector organ, the lung, and in the lung draining lymph nodes (LN). ¶ Materials and Subjects: In BALB/c mice pathophysiological parameters were measured in vivo, and lung draining LN and lung cells were restimulated in vitro. ¶ Treatment: Mice were sensitized with ovalbumin and repeatedly challenged with ovalbumin or saline inhalation. ¶ Methods: Airway reactivity, inflammation in the airways, serum levels of IgE were measured, and cytokine levels and proliferative responses were determined in antigen-stimulated lymphocyte cultures. ¶ Results and Conclusions: Sensitization results in antigen-specific Th0-like LN cells, despite the presence of antigen-specific IgE. Repeated antigen inhalation induced airway hyperresponsiveness and eosinophil infiltration concomitant with a shift towards Th2 cytokine production exclusively by lung draining LN T cells. Furthermore, these airway symptoms are associated with antigen-specific CD4+ effector T cells in the airway tissue producing only IL-5, but not IL-4, which are unable to proliferate.
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