Allergic pulmonary inflammation in mice is dependent on eosinophil-induced recruitment of effector T cells

Elizabeth A. Jacobsen, Sergei I. Ochkur, Ralph S. Pero, Anna G. Taranova, Cheryl A. Protheroe, Dana C. Colbert, Nancy A. Lee, James J. Lee

Research output: Contribution to journalArticle

177 Scopus citations

Abstract

The current paradigm surrounding allergen-mediated T helper type 2 (Th2) immune responses in the lung suggests an almost hegemonic role for T cells. Our studies propose an alternative hypothesis implicating eosinophils in the regulation of pulmonary T cell responses. In particular, ovalbumin (OVA)-sensitized/challenged mice devoid of eosinophils (the transgenic line PHIL) have reduced airway levels of Th2 cytokines relative to the OVA-treated wild type that correlated with a reduced ability to recruit effector T cells to the lung. Adoptive transfer of Th2-polarized OVA-specific transgenic T cells (OT-II) alone into OVA-challenged PHIL recipient mice failed to restore Th2 cytokines, airway histopathologies, and, most importantly, the recruitment of pulmonary effector T cells. In contrast, the combined transfer of OT-II cells and eosinophils into PHIL mice resulted in the accumulation of effector T cells and a concomitant increase in both airway Th2 immune responses and histopathologies. Moreover, we show that eosinophils elicit the expression of the Th2 chemokines thymus- and activation-regulated chemokine/CCL17 and macrophage-derived chemokine/CCL22 in the lung after allergen challenge, and blockade of these chemokines inhibited the recruitment of effector T cells. In summary, the data suggest that pulmonary eosinophils are required for the localized recruitment of effector T cells. JEM

Original languageEnglish (US)
Pages (from-to)699-710
Number of pages12
JournalJournal of Experimental Medicine
Volume205
Issue number3
DOIs
StatePublished - Mar 17 2008

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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