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

Authors: Jacobsen, EA  Ochkur, SI  Pero, RS  Taranova, AG  Protheroe, CA  Colbert, DC  Lee, NA  Lee, JJ 
Citation: Jacobsen EA, etal., J Exp Med. 2008 Mar 17;205(3):699-710. Epub 2008 Mar 3.
Pubmed: (View Article at PubMed) PMID:18316417
DOI: Full-text: DOI:10.1084/jem.20071840

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.

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CRRD Object Information
CRRD ID: 4891474
Created: 2011-01-14
Species: All species
Last Modified: 2011-01-14
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.