<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Shalaby KH</submitter><funding>Intramural NIH HHS</funding><funding>NULL</funding><pagination>1229-1242.e6</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5951733</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>142(4)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Mechanisms that elicit mucosal T&lt;sub>H&lt;/sub>17 cell responses have been described, yet how these cells are sustained in chronically inflamed tissues remains unclear.&lt;h4>Objective&lt;/h4>We sought to understand whether maintenance of lung T&lt;sub>H&lt;/sub>17 inflammation requires environmental agents in addition to antigen and to identify the lung antigen-presenting cell (APC) types that sustain the self-renewal of T&lt;sub>H&lt;/sub>17 cells.&lt;h4>Methods&lt;/h4>Animals were exposed repeatedly to aspiration of ovalbumin alone or together with environmental adjuvants, including common house dust extract (HDE), to test their role in maintaining lung inflammation. Alternatively, antigen-specific effector/memory T&lt;sub>H&lt;/sub>17 cells, generated in culture with CD4&lt;sup>+&lt;/sup> T cells from Il1</pubmed_abstract><journal>The Journal of allergy and clinical immunology</journal><pubmed_title>Pathogenic T&amp;lt;sub&amp;gt;H&amp;lt;/sub&amp;gt;17 inflammation is sustained in the lungs by conventional dendritic cells and Toll-like receptor 4 signaling.</pubmed_title><pmcid>PMC5951733</pmcid><funding_grant_id>ZIA ES102025-09</funding_grant_id><funding_grant_id>Z01 ES102025</funding_grant_id><funding_grant_id>ZIA ES102025</funding_grant_id><pubmed_authors>Lyons-Cohen MR</pubmed_authors><pubmed_authors>Whitehead GS</pubmed_authors><pubmed_authors>Shalaby KH</pubmed_authors><pubmed_authors>Prinz I</pubmed_authors><pubmed_authors>Cook DN</pubmed_authors><pubmed_authors>Nakano H</pubmed_authors><pubmed_authors>Thomas SY</pubmed_authors></additional><is_claimable>false</is_claimable><name>Pathogenic T&amp;lt;sub&amp;gt;H&amp;lt;/sub&amp;gt;17 inflammation is sustained in the lungs by conventional dendritic cells and Toll-like receptor 4 signaling.</name><description>&lt;h4>Background&lt;/h4>Mechanisms that elicit mucosal T&lt;sub>H&lt;/sub>17 cell responses have been described, yet how these cells are sustained in chronically inflamed tissues remains unclear.&lt;h4>Objective&lt;/h4>We sought to understand whether maintenance of lung T&lt;sub>H&lt;/sub>17 inflammation requires environmental agents in addition to antigen and to identify the lung antigen-presenting cell (APC) types that sustain the self-renewal of T&lt;sub>H&lt;/sub>17 cells.&lt;h4>Methods&lt;/h4>Animals were exposed repeatedly to aspiration of ovalbumin alone or together with environmental adjuvants, including common house dust extract (HDE), to test their role in maintaining lung inflammation. Alternatively, antigen-specific effector/memory T&lt;sub>H&lt;/sub>17 cells, generated in culture with CD4&lt;sup>+&lt;/sup> T cells from Il1</description><dates><release>2018-01-01T00:00:00Z</release><publication>2018 Oct</publication><modification>2026-04-13T07:15:37.633Z</modification><creation>2019-03-26T23:59:40Z</creation></dates><accession>S-EPMC5951733</accession><cross_references><pubmed>29154958</pubmed><doi>10.1016/j.jaci.2017.10.023</doi></cross_references></HashMap>