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Group 2 innate lymphoid cells license dendritic cells to potentiate memory T helper 2 cell responses
Rapid memory CD4(+) T helper 2 (T(H)2) cell activation during allergic inflammation requires their recruitment into the affected tissue. Here we demonstrate that group 2 innate lymphoid cells (ILC2) play a critical role in memory T(H)2 cell responses, with targeted ILC2 depletion profoundly impairin...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4685755/ https://www.ncbi.nlm.nih.gov/pubmed/26523868 http://dx.doi.org/10.1038/ni.3294 |
Sumario: | Rapid memory CD4(+) T helper 2 (T(H)2) cell activation during allergic inflammation requires their recruitment into the affected tissue. Here we demonstrate that group 2 innate lymphoid cells (ILC2) play a critical role in memory T(H)2 cell responses, with targeted ILC2 depletion 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 IRF4(+)CD11b(+)CD103(−) dendritic cells (DCs) to produce the T(H)2 cell-attracting chemokine CCL17. Consequently, the sentinel function of DCs is contingent on ILC2s for the generation of an efficient memory T(H)2 cell response. These results elucidate a key new innate mechanism in the regulation of the immune memory response to allergens. |
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