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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...

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Detalles Bibliográficos
Autores principales: Halim, Timotheus YF, Hwang, You Yi, Scanlon, Seth T, Zaghouani, Habib, Garbi, Natalio, Fallon, Padraic G, McKenzie, Andrew NJ
Formato: Online Artículo Texto
Lenguaje:English
Publicado: 2015
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
Descripción
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.