<HashMap><database>biostudies-literature</database><scores><citationCount>0</citationCount><reanalysisCount>0</reanalysisCount><viewCount>46</viewCount><searchCount>0</searchCount></scores><additional><submitter>Halim TY</submitter><funding>Medical Research Council</funding><funding>Wellcome Trust</funding><funding>Canadian Institutes of Health Research</funding><pagination>57-64</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4685755</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>17(1)</volume><pubmed_abstract>Rapid activation of memory CD4(+) T helper 2 (TH2) 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 TH2 cell responses, with targeted depletion of ILC2 cells profoundly impairing TH2 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 TH2 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 TH2 cell response. These results elucidate a key innate mechanism in the regulation of the immune memory response to allergens.</pubmed_abstract><journal>Nature immunology</journal><pubmed_title>Group 2 innate lymphoid cells license dendritic cells to potentiate memory TH2 cell responses.</pubmed_title><pmcid>PMC4685755</pmcid><funding_grant_id>UI05178805</funding_grant_id><funding_grant_id>MC_U105178805</funding_grant_id><funding_grant_id>100963/Z/13/Z</funding_grant_id><funding_grant_id>100963</funding_grant_id><pubmed_authors>Scanlon ST</pubmed_authors><pubmed_authors>McKenzie AN</pubmed_authors><pubmed_authors>Zaghouani H</pubmed_authors><pubmed_authors>Halim TY</pubmed_authors><pubmed_authors>Hwang YY</pubmed_authors><pubmed_authors>Garbi N</pubmed_authors><pubmed_authors>Fallon PG</pubmed_authors><view_count>46</view_count></additional><is_claimable>false</is_claimable><name>Group 2 innate lymphoid cells license dendritic cells to potentiate memory TH2 cell responses.</name><description>Rapid activation of memory CD4(+) T helper 2 (TH2) 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 TH2 cell responses, with targeted depletion of ILC2 cells profoundly impairing TH2 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 TH2 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 TH2 cell response. These results elucidate a key innate mechanism in the regulation of the immune memory response to allergens.</description><dates><release>2016-01-01T00:00:00Z</release><publication>2016 Jan</publication><modification>2021-02-20T07:54:52Z</modification><creation>2019-03-27T02:05:31Z</creation></dates><accession>S-EPMC4685755</accession><cross_references><pubmed>26523868</pubmed><doi>10.1038/ni.3294</doi></cross_references></HashMap>