Journal
NATURE IMMUNOLOGY
Volume 17, Issue 1, Pages 57-+Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.3294
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Funding
- UK Medical Research Council [UI05178805]
- Wellcome Trust [100963]
- Science Foundation Ireland
- National Children's Research Centre
- A-STAR
- Canadian Institutes of Health Research
- DFG
- MRC [MC_U105178805] Funding Source: UKRI
- Medical Research Council [MC_U105178805] Funding Source: researchfish
- Wellcome Trust [100963/Z/13/Z] Funding Source: researchfish
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Rapid activation of memory CD4(+) T helper 2 (T(H)2) cells during allergic inflammation requires their recruitment into the affected tissue. Here we demonstrate that group 2 innate lymphoid (ILC2) cells have a crucial role in memory T(H)2 cell responses, with targeted depletion of ILC2 cells profoundly impairing T(H)2 cell localization to the lungs and skin of sensitized mice after allergen re-challenge. ILC2-derived interleukin 13 (IL-13) is critical for eliciting production of the T(H)2 cell-attracting chemokine CCL17 by IRF4(+)CD11b(+)CD103(-) dendritic cells (DCs). Consequently, the sentinel function of DCs is contingent on ILC2 cells for the generation of an efficient memory T(H)2 cell response. These results elucidate a key innate mechanism in the regulation of the immune memory response to allergens.
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