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English Abstract
Journal Article
Research Support, Non-U.S. Gov't
[Endobronchial eosinophils preferentially stimulate T helper cell type 2 responses].
Zhonghua Yi Xue za Zhi [Chinese medical journal] 2003 December 26
OBJECTIVE: The aim of the present study was to evaluate whether eosinophils within the tracheobronchial lumen can stimulate Th2 cell expansion by presenting antigen both in vitro and in vivo.
METHODS: Airway eosinophils were recovered from ovalbumin-sensitized and -challenged BALB/c mice, these eosinophils were then cocultured with sensitized CD4(+) cells in the absence or presence of anti-CD80 or/and -CD86 monoclonal antibodies. Airway eosinophils were instilled into the trachea of sensitized mice, At 3 d thereafter, the draining paratracheal lymph nodes were removed and teased into cell suspensions for culture. Cell-free culture supernatants were collected for detection of cytokines.
RESULTS: Our data showed that airway eosinophils, recovered following inhalational ovalbumin challenge in sensitized mice functioned as CD80- and CD86-dependent antigen-presenting cells to stimulate sensitized CD4(+) lymphocytes to produce IL-4, IL-5 and IL-13, but not interferon-gamma (IFN-gamma) in vitro assay. When instilled intratracheally in ovalbumin-sensitized recipient mice, these antigen-loaded eosinophils migrated into draining paratracheal lymph nodes primed Th2 cells in vivo for IL-4, IL-5 and IL-13, but not IFN-gamma, production during the in vitro culture that was also CD80- and CD86-dependent.
CONCLUSIONS: We concluded that eosinophils within the lumina of airways could process inhaled antigen function in vitro and in vivo as antigen-presenting cells to promote expansion of Th2 cells. This investigation highlights the potential of eosinophils to not only act as terminal effector cells but also to actively modulate immune responses by amplifying Th2 cell responses.
METHODS: Airway eosinophils were recovered from ovalbumin-sensitized and -challenged BALB/c mice, these eosinophils were then cocultured with sensitized CD4(+) cells in the absence or presence of anti-CD80 or/and -CD86 monoclonal antibodies. Airway eosinophils were instilled into the trachea of sensitized mice, At 3 d thereafter, the draining paratracheal lymph nodes were removed and teased into cell suspensions for culture. Cell-free culture supernatants were collected for detection of cytokines.
RESULTS: Our data showed that airway eosinophils, recovered following inhalational ovalbumin challenge in sensitized mice functioned as CD80- and CD86-dependent antigen-presenting cells to stimulate sensitized CD4(+) lymphocytes to produce IL-4, IL-5 and IL-13, but not interferon-gamma (IFN-gamma) in vitro assay. When instilled intratracheally in ovalbumin-sensitized recipient mice, these antigen-loaded eosinophils migrated into draining paratracheal lymph nodes primed Th2 cells in vivo for IL-4, IL-5 and IL-13, but not IFN-gamma, production during the in vitro culture that was also CD80- and CD86-dependent.
CONCLUSIONS: We concluded that eosinophils within the lumina of airways could process inhaled antigen function in vitro and in vivo as antigen-presenting cells to promote expansion of Th2 cells. This investigation highlights the potential of eosinophils to not only act as terminal effector cells but also to actively modulate immune responses by amplifying Th2 cell responses.
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