Tumor necrosis factor-related apoptosis-inducing ligand mediates the resolution of allergic airway inflammation induced by chronic allergen inhalation
Allergic asthma can vanish over time either spontaneously or induced by allergen-specific immunotherapy. In mice with established airway allergic inflammation, chronic intranasal (IN) allergen challenges decreases progressively airway allergic inflammation. Here we compared the contribution of diffe...
Gespeichert in:
Veröffentlicht in: | Mucosal immunology 2014-09, Vol.7 (5), p.1199-1208 |
---|---|
Hauptverfasser: | , , , , , , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
container_end_page | 1208 |
---|---|
container_issue | 5 |
container_start_page | 1199 |
container_title | Mucosal immunology |
container_volume | 7 |
creator | Faustino, L Fonseca, D M Florsheim, E B Resende, R R Lepique, A P Faquim-Mauro, E Gomes, E Silva, J S Yagita, H Russo, M |
description | Allergic asthma can vanish over time either spontaneously or induced by allergen-specific immunotherapy. In mice with established airway allergic inflammation, chronic intranasal (IN) allergen challenges decreases progressively airway allergic inflammation. Here we compared the contribution of different regulatory pathways that could be associated with this phenomenon, known as local inhalational tolerance. We found that inhalational tolerance was not associated with increased number of regulatory T cells or suppressive cytokines. Instead, it was associated with increased apoptosis of airway inflammatory leukocytes revealed by annexin-V staining and the expression of apical caspase 8 and effector caspase 3. Also, the transition from acute to chronic phase was associated with a shift in the expression of pro-allergic to pro-apoptotic molecules. The tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) was found to be a key molecule in mediating resolution of allergic inflammation because anti-TRAIL treatment blocked apoptosis and increased the infiltration of T helper type 2 (Th2) cells and eosinophils. Notably, repeated IN treatment with recombinant TRAIL in established airway allergic inflammation augmented leukocyte apoptosis and decreased the frequency of interleukin-5-producing Th2 cells and eosinophils to airways. Our data indicate that TRAIL signaling is sufficient for downmodulation of allergic airway disease, suggesting a potential therapeutic use of TRAIL for asthma treatment. |
doi_str_mv | 10.1038/mi.2014.9 |
format | Article |
fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1554941724</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>4030226041</sourcerecordid><originalsourceid>FETCH-LOGICAL-c383t-2761ff2b35e17a2108c339a816e1d69f4e13e44e580c9f05792f371f91e889953</originalsourceid><addsrcrecordid>eNplkctq3DAUhkVIaNIki7xAEWSTFjzVxbKlZQnpBQLZpGujkY9mFGRpKtmEeZE-b2VPGkK7kQTfx3_E-RG6omRFCZefB7dihNYrdYTOqOKi4rVojpc3rwij6hS9z_mJkIYQwd-hU1a4koSdod-P0xATDmBSzC5jq80YU5XA6xF6rHdxN86gcqGfjAsb7N1Ghx4P0LuiZDxuASfI0U-jiwFHi7X3kDbOYO3Ss95jF6zXw6AXvuSU5PUem22KYdYWH2a21X7RLtCJ1T7D5ct9jn5-vXu8_V7dP3z7cfvlvjJc8rFibUOtZWsugLaaUSIN50pL2gDtG2VroBzqGoQkRlkiWsUsb6lVFKRUSvBzdHPI3aX4a4I8doPLBrzXAeKUOypErWrasrqo1_-oT3FKofyuo63kpGHlLNbHgzXvMyew3S65Qad9R0k3l1UGdHNZnSruh5fEaV3W-Wr-bacInw5CLihsIL0Z-V_aH-hTn68</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1783062783</pqid></control><display><type>article</type><title>Tumor necrosis factor-related apoptosis-inducing ligand mediates the resolution of allergic airway inflammation induced by chronic allergen inhalation</title><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>ProQuest Central UK/Ireland</source><source>Alma/SFX Local Collection</source><creator>Faustino, L ; Fonseca, D M ; Florsheim, E B ; Resende, R R ; Lepique, A P ; Faquim-Mauro, E ; Gomes, E ; Silva, J S ; Yagita, H ; Russo, M</creator><creatorcontrib>Faustino, L ; Fonseca, D M ; Florsheim, E B ; Resende, R R ; Lepique, A P ; Faquim-Mauro, E ; Gomes, E ; Silva, J S ; Yagita, H ; Russo, M</creatorcontrib><description>Allergic asthma can vanish over time either spontaneously or induced by allergen-specific immunotherapy. In mice with established airway allergic inflammation, chronic intranasal (IN) allergen challenges decreases progressively airway allergic inflammation. Here we compared the contribution of different regulatory pathways that could be associated with this phenomenon, known as local inhalational tolerance. We found that inhalational tolerance was not associated with increased number of regulatory T cells or suppressive cytokines. Instead, it was associated with increased apoptosis of airway inflammatory leukocytes revealed by annexin-V staining and the expression of apical caspase 8 and effector caspase 3. Also, the transition from acute to chronic phase was associated with a shift in the expression of pro-allergic to pro-apoptotic molecules. The tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) was found to be a key molecule in mediating resolution of allergic inflammation because anti-TRAIL treatment blocked apoptosis and increased the infiltration of T helper type 2 (Th2) cells and eosinophils. Notably, repeated IN treatment with recombinant TRAIL in established airway allergic inflammation augmented leukocyte apoptosis and decreased the frequency of interleukin-5-producing Th2 cells and eosinophils to airways. Our data indicate that TRAIL signaling is sufficient for downmodulation of allergic airway disease, suggesting a potential therapeutic use of TRAIL for asthma treatment.</description><identifier>ISSN: 1933-0219</identifier><identifier>EISSN: 1935-3456</identifier><identifier>DOI: 10.1038/mi.2014.9</identifier><identifier>PMID: 24569802</identifier><language>eng</language><publisher>New York: Nature Publishing Group US</publisher><subject>631/250/249/2510/31 ; 631/250/249/2510/9 ; 631/250/347 ; 631/80/86 ; Allergens - immunology ; Allergology ; Animals ; Antibodies ; Antibodies, Monoclonal - immunology ; Apoptosis - immunology ; Biomedical and Life Sciences ; Biomedicine ; Caspase 3 - genetics ; Caspase 3 - metabolism ; Caspase 8 - genetics ; Caspase 8 - metabolism ; Chronic Disease ; Female ; Gastroenterology ; Gene Expression Regulation - immunology ; Immunology ; Inflammation - drug therapy ; Inflammation - immunology ; Lung - immunology ; Lung - physiopathology ; Mice ; Mice, Knockout ; Recombinant Proteins - genetics ; Respiratory Hypersensitivity - drug therapy ; Respiratory Hypersensitivity - immunology ; Th2 Cells - immunology ; TNF-Related Apoptosis-Inducing Ligand - genetics ; TNF-Related Apoptosis-Inducing Ligand - metabolism ; TNF-Related Apoptosis-Inducing Ligand - therapeutic use</subject><ispartof>Mucosal immunology, 2014-09, Vol.7 (5), p.1199-1208</ispartof><rights>Society for Mucosal Immunology 2014</rights><rights>Copyright Nature Publishing Group Sep 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c383t-2761ff2b35e17a2108c339a816e1d69f4e13e44e580c9f05792f371f91e889953</citedby><cites>FETCH-LOGICAL-c383t-2761ff2b35e17a2108c339a816e1d69f4e13e44e580c9f05792f371f91e889953</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.proquest.com/docview/1783062783?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,64385,64387,64389,72469</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24569802$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Faustino, L</creatorcontrib><creatorcontrib>Fonseca, D M</creatorcontrib><creatorcontrib>Florsheim, E B</creatorcontrib><creatorcontrib>Resende, R R</creatorcontrib><creatorcontrib>Lepique, A P</creatorcontrib><creatorcontrib>Faquim-Mauro, E</creatorcontrib><creatorcontrib>Gomes, E</creatorcontrib><creatorcontrib>Silva, J S</creatorcontrib><creatorcontrib>Yagita, H</creatorcontrib><creatorcontrib>Russo, M</creatorcontrib><title>Tumor necrosis factor-related apoptosis-inducing ligand mediates the resolution of allergic airway inflammation induced by chronic allergen inhalation</title><title>Mucosal immunology</title><addtitle>Mucosal Immunol</addtitle><addtitle>Mucosal Immunol</addtitle><description>Allergic asthma can vanish over time either spontaneously or induced by allergen-specific immunotherapy. In mice with established airway allergic inflammation, chronic intranasal (IN) allergen challenges decreases progressively airway allergic inflammation. Here we compared the contribution of different regulatory pathways that could be associated with this phenomenon, known as local inhalational tolerance. We found that inhalational tolerance was not associated with increased number of regulatory T cells or suppressive cytokines. Instead, it was associated with increased apoptosis of airway inflammatory leukocytes revealed by annexin-V staining and the expression of apical caspase 8 and effector caspase 3. Also, the transition from acute to chronic phase was associated with a shift in the expression of pro-allergic to pro-apoptotic molecules. The tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) was found to be a key molecule in mediating resolution of allergic inflammation because anti-TRAIL treatment blocked apoptosis and increased the infiltration of T helper type 2 (Th2) cells and eosinophils. Notably, repeated IN treatment with recombinant TRAIL in established airway allergic inflammation augmented leukocyte apoptosis and decreased the frequency of interleukin-5-producing Th2 cells and eosinophils to airways. Our data indicate that TRAIL signaling is sufficient for downmodulation of allergic airway disease, suggesting a potential therapeutic use of TRAIL for asthma treatment.</description><subject>631/250/249/2510/31</subject><subject>631/250/249/2510/9</subject><subject>631/250/347</subject><subject>631/80/86</subject><subject>Allergens - immunology</subject><subject>Allergology</subject><subject>Animals</subject><subject>Antibodies</subject><subject>Antibodies, Monoclonal - immunology</subject><subject>Apoptosis - immunology</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Caspase 3 - genetics</subject><subject>Caspase 3 - metabolism</subject><subject>Caspase 8 - genetics</subject><subject>Caspase 8 - metabolism</subject><subject>Chronic Disease</subject><subject>Female</subject><subject>Gastroenterology</subject><subject>Gene Expression Regulation - immunology</subject><subject>Immunology</subject><subject>Inflammation - drug therapy</subject><subject>Inflammation - immunology</subject><subject>Lung - immunology</subject><subject>Lung - physiopathology</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Recombinant Proteins - genetics</subject><subject>Respiratory Hypersensitivity - drug therapy</subject><subject>Respiratory Hypersensitivity - immunology</subject><subject>Th2 Cells - immunology</subject><subject>TNF-Related Apoptosis-Inducing Ligand - genetics</subject><subject>TNF-Related Apoptosis-Inducing Ligand - metabolism</subject><subject>TNF-Related Apoptosis-Inducing Ligand - therapeutic use</subject><issn>1933-0219</issn><issn>1935-3456</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNplkctq3DAUhkVIaNIki7xAEWSTFjzVxbKlZQnpBQLZpGujkY9mFGRpKtmEeZE-b2VPGkK7kQTfx3_E-RG6omRFCZefB7dihNYrdYTOqOKi4rVojpc3rwij6hS9z_mJkIYQwd-hU1a4koSdod-P0xATDmBSzC5jq80YU5XA6xF6rHdxN86gcqGfjAsb7N1Ghx4P0LuiZDxuASfI0U-jiwFHi7X3kDbOYO3Ss95jF6zXw6AXvuSU5PUem22KYdYWH2a21X7RLtCJ1T7D5ct9jn5-vXu8_V7dP3z7cfvlvjJc8rFibUOtZWsugLaaUSIN50pL2gDtG2VroBzqGoQkRlkiWsUsb6lVFKRUSvBzdHPI3aX4a4I8doPLBrzXAeKUOypErWrasrqo1_-oT3FKofyuo63kpGHlLNbHgzXvMyew3S65Qad9R0k3l1UGdHNZnSruh5fEaV3W-Wr-bacInw5CLihsIL0Z-V_aH-hTn68</recordid><startdate>20140901</startdate><enddate>20140901</enddate><creator>Faustino, L</creator><creator>Fonseca, D M</creator><creator>Florsheim, E B</creator><creator>Resende, R R</creator><creator>Lepique, A P</creator><creator>Faquim-Mauro, E</creator><creator>Gomes, E</creator><creator>Silva, J S</creator><creator>Yagita, H</creator><creator>Russo, M</creator><general>Nature Publishing Group US</general><general>Elsevier Limited</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20140901</creationdate><title>Tumor necrosis factor-related apoptosis-inducing ligand mediates the resolution of allergic airway inflammation induced by chronic allergen inhalation</title><author>Faustino, L ; Fonseca, D M ; Florsheim, E B ; Resende, R R ; Lepique, A P ; Faquim-Mauro, E ; Gomes, E ; Silva, J S ; Yagita, H ; Russo, M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c383t-2761ff2b35e17a2108c339a816e1d69f4e13e44e580c9f05792f371f91e889953</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>631/250/249/2510/31</topic><topic>631/250/249/2510/9</topic><topic>631/250/347</topic><topic>631/80/86</topic><topic>Allergens - immunology</topic><topic>Allergology</topic><topic>Animals</topic><topic>Antibodies</topic><topic>Antibodies, Monoclonal - immunology</topic><topic>Apoptosis - immunology</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Caspase 3 - genetics</topic><topic>Caspase 3 - metabolism</topic><topic>Caspase 8 - genetics</topic><topic>Caspase 8 - metabolism</topic><topic>Chronic Disease</topic><topic>Female</topic><topic>Gastroenterology</topic><topic>Gene Expression Regulation - immunology</topic><topic>Immunology</topic><topic>Inflammation - drug therapy</topic><topic>Inflammation - immunology</topic><topic>Lung - immunology</topic><topic>Lung - physiopathology</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Recombinant Proteins - genetics</topic><topic>Respiratory Hypersensitivity - drug therapy</topic><topic>Respiratory Hypersensitivity - immunology</topic><topic>Th2 Cells - immunology</topic><topic>TNF-Related Apoptosis-Inducing Ligand - genetics</topic><topic>TNF-Related Apoptosis-Inducing Ligand - metabolism</topic><topic>TNF-Related Apoptosis-Inducing Ligand - therapeutic use</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Faustino, L</creatorcontrib><creatorcontrib>Fonseca, D M</creatorcontrib><creatorcontrib>Florsheim, E B</creatorcontrib><creatorcontrib>Resende, R R</creatorcontrib><creatorcontrib>Lepique, A P</creatorcontrib><creatorcontrib>Faquim-Mauro, E</creatorcontrib><creatorcontrib>Gomes, E</creatorcontrib><creatorcontrib>Silva, J S</creatorcontrib><creatorcontrib>Yagita, H</creatorcontrib><creatorcontrib>Russo, M</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Mucosal immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Faustino, L</au><au>Fonseca, D M</au><au>Florsheim, E B</au><au>Resende, R R</au><au>Lepique, A P</au><au>Faquim-Mauro, E</au><au>Gomes, E</au><au>Silva, J S</au><au>Yagita, H</au><au>Russo, M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Tumor necrosis factor-related apoptosis-inducing ligand mediates the resolution of allergic airway inflammation induced by chronic allergen inhalation</atitle><jtitle>Mucosal immunology</jtitle><stitle>Mucosal Immunol</stitle><addtitle>Mucosal Immunol</addtitle><date>2014-09-01</date><risdate>2014</risdate><volume>7</volume><issue>5</issue><spage>1199</spage><epage>1208</epage><pages>1199-1208</pages><issn>1933-0219</issn><eissn>1935-3456</eissn><abstract>Allergic asthma can vanish over time either spontaneously or induced by allergen-specific immunotherapy. In mice with established airway allergic inflammation, chronic intranasal (IN) allergen challenges decreases progressively airway allergic inflammation. Here we compared the contribution of different regulatory pathways that could be associated with this phenomenon, known as local inhalational tolerance. We found that inhalational tolerance was not associated with increased number of regulatory T cells or suppressive cytokines. Instead, it was associated with increased apoptosis of airway inflammatory leukocytes revealed by annexin-V staining and the expression of apical caspase 8 and effector caspase 3. Also, the transition from acute to chronic phase was associated with a shift in the expression of pro-allergic to pro-apoptotic molecules. The tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) was found to be a key molecule in mediating resolution of allergic inflammation because anti-TRAIL treatment blocked apoptosis and increased the infiltration of T helper type 2 (Th2) cells and eosinophils. Notably, repeated IN treatment with recombinant TRAIL in established airway allergic inflammation augmented leukocyte apoptosis and decreased the frequency of interleukin-5-producing Th2 cells and eosinophils to airways. Our data indicate that TRAIL signaling is sufficient for downmodulation of allergic airway disease, suggesting a potential therapeutic use of TRAIL for asthma treatment.</abstract><cop>New York</cop><pub>Nature Publishing Group US</pub><pmid>24569802</pmid><doi>10.1038/mi.2014.9</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 1933-0219 |
ispartof | Mucosal immunology, 2014-09, Vol.7 (5), p.1199-1208 |
issn | 1933-0219 1935-3456 |
language | eng |
recordid | cdi_proquest_miscellaneous_1554941724 |
source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; ProQuest Central UK/Ireland; Alma/SFX Local Collection |
subjects | 631/250/249/2510/31 631/250/249/2510/9 631/250/347 631/80/86 Allergens - immunology Allergology Animals Antibodies Antibodies, Monoclonal - immunology Apoptosis - immunology Biomedical and Life Sciences Biomedicine Caspase 3 - genetics Caspase 3 - metabolism Caspase 8 - genetics Caspase 8 - metabolism Chronic Disease Female Gastroenterology Gene Expression Regulation - immunology Immunology Inflammation - drug therapy Inflammation - immunology Lung - immunology Lung - physiopathology Mice Mice, Knockout Recombinant Proteins - genetics Respiratory Hypersensitivity - drug therapy Respiratory Hypersensitivity - immunology Th2 Cells - immunology TNF-Related Apoptosis-Inducing Ligand - genetics TNF-Related Apoptosis-Inducing Ligand - metabolism TNF-Related Apoptosis-Inducing Ligand - therapeutic use |
title | Tumor necrosis factor-related apoptosis-inducing ligand mediates the resolution of allergic airway inflammation induced by chronic allergen inhalation |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-04T02%3A18%3A57IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Tumor%20necrosis%20factor-related%20apoptosis-inducing%20ligand%20mediates%20the%20resolution%20of%20allergic%20airway%20inflammation%20induced%20by%20chronic%20allergen%20inhalation&rft.jtitle=Mucosal%20immunology&rft.au=Faustino,%20L&rft.date=2014-09-01&rft.volume=7&rft.issue=5&rft.spage=1199&rft.epage=1208&rft.pages=1199-1208&rft.issn=1933-0219&rft.eissn=1935-3456&rft_id=info:doi/10.1038/mi.2014.9&rft_dat=%3Cproquest_cross%3E4030226041%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1783062783&rft_id=info:pmid/24569802&rfr_iscdi=true |