ILC2s activated by IL-25 promote antigen-specific Th2 and Th9 functions that contribute to the control of Trichinella spiralis infection
IL-25, an IL-17 family cytokine, derived from epithelial cells was shown to regulate Th2- and Th9-type immune responses. We previously reported that IL-25 was important in promoting efficient protective immunity against T. spiralis infection; however, the cellular targets of IL-25 to elicit type-2 i...
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| creator | Angkasekwinai, Pornpimon Sodthawon, Wichuda Jeerawattanawart, Siranart Hansakon, Adithap Pattanapanyasat, Kovit Wang, Yui-Hsi |
| description | IL-25, an IL-17 family cytokine, derived from epithelial cells was shown to regulate Th2- and Th9-type immune responses. We previously reported that IL-25 was important in promoting efficient protective immunity against T. spiralis infection; however, the cellular targets of IL-25 to elicit type-2 immunity during infection have not yet been addressed. Here, we investigated IL-25-responding cells and their involvement in mediating type-2 immune response during T. spiralis infection. ILC2 and CD4+ Th2 cells residing in the gastrointestinal tract of T. spiralis infected mice were found to express high levels of surface interleukin-17 receptor B (IL-17RB), a component of the IL-25 receptor. Following T. spiralis infection, activated ILC2s upregulated surface MHCII expression and enhanced capacity of effector T helper cell in producing antigen-specific Th2 and Th9 cytokines through MHCII-dependent interactions. Reciprocally, lack of CD4+ T helper cells impaired ILC2 function to produce type 2-associated cytokines in responding to IL-25 during T. spiralis infection. Furthermore, mice deficient in IL-17RB showed markedly reduced ILC2 numbers and antigen-specific Th2 and Th9 cytokine production during T. spiralis infection. The Il17rb-/- mice failed to mount effective antigen specific Th2 and Th9 functions resulting in diminished goblet cell and mast cell responses, leading to delayed worm expulsion in the intestines and muscles. Thus, our data indicated that ILC2s and CD4+ Th2 cells are the predominant cellular targets of IL-25 following T. spiralis infection and their collaborative interactions may play a key role in mounting effective antigen-specific Th2 and Th9 cytokine responses against T. spiralis infection. |
| doi_str_mv | 10.1371/journal.pone.0184684 |
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We previously reported that IL-25 was important in promoting efficient protective immunity against T. spiralis infection; however, the cellular targets of IL-25 to elicit type-2 immunity during infection have not yet been addressed. Here, we investigated IL-25-responding cells and their involvement in mediating type-2 immune response during T. spiralis infection. ILC2 and CD4+ Th2 cells residing in the gastrointestinal tract of T. spiralis infected mice were found to express high levels of surface interleukin-17 receptor B (IL-17RB), a component of the IL-25 receptor. Following T. spiralis infection, activated ILC2s upregulated surface MHCII expression and enhanced capacity of effector T helper cell in producing antigen-specific Th2 and Th9 cytokines through MHCII-dependent interactions. Reciprocally, lack of CD4+ T helper cells impaired ILC2 function to produce type 2-associated cytokines in responding to IL-25 during T. spiralis infection. Furthermore, mice deficient in IL-17RB showed markedly reduced ILC2 numbers and antigen-specific Th2 and Th9 cytokine production during T. spiralis infection. The Il17rb-/- mice failed to mount effective antigen specific Th2 and Th9 functions resulting in diminished goblet cell and mast cell responses, leading to delayed worm expulsion in the intestines and muscles. Thus, our data indicated that ILC2s and CD4+ Th2 cells are the predominant cellular targets of IL-25 following T. spiralis infection and their collaborative interactions may play a key role in mounting effective antigen-specific Th2 and Th9 cytokine responses against T. spiralis infection.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0184684</identifier><identifier>PMID: 28898280</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Animals ; Antigens ; Biology and Life Sciences ; CD4 antigen ; Cells, Cultured ; Cloning ; Cytokines ; Development and progression ; Epithelial cells ; Expulsion ; Gastrointestinal tract ; Genes, MHC Class II ; Genetic aspects ; Goblet Cells - immunology ; Health aspects ; Health sciences ; Helper cells ; Hospitals ; Immune response ; Immune system ; Immunity ; Immunity, Innate ; Immunology ; Infections ; Interleukin 1 ; Interleukin 17 ; Interleukin-10 - metabolism ; Interleukin-17 - metabolism ; Interleukins ; Intestine ; Laboratory animals ; Lymphocytes ; Lymphocytes T ; Mast Cells - immunology ; Medical research ; Medical technology ; Medicine and Health Sciences ; Mice ; Mice, Inbred BALB C ; Muscles ; Physiological aspects ; Receptors, Interleukin-17 - genetics ; Receptors, Interleukin-17 - metabolism ; Studies ; T cells ; Th2 Cells - immunology ; Trichinella spiralis ; Trichinella spiralis - immunology ; Trichinellosis - immunology ; Trichinosis</subject><ispartof>PloS one, 2017-09, Vol.12 (9), p.e0184684-e0184684</ispartof><rights>COPYRIGHT 2017 Public Library of Science</rights><rights>2017 Angkasekwinai et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2017 Angkasekwinai et al 2017 Angkasekwinai et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-b48afab9f4ac6b3b34e5f46b61aa7bcc95c245fab4b51469ac99d27f337a9a153</citedby><cites>FETCH-LOGICAL-c692t-b48afab9f4ac6b3b34e5f46b61aa7bcc95c245fab4b51469ac99d27f337a9a153</cites><orcidid>0000-0003-0303-9544</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5595335/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5595335/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79342,79343</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28898280$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Angkasekwinai, Pornpimon</creatorcontrib><creatorcontrib>Sodthawon, Wichuda</creatorcontrib><creatorcontrib>Jeerawattanawart, Siranart</creatorcontrib><creatorcontrib>Hansakon, Adithap</creatorcontrib><creatorcontrib>Pattanapanyasat, Kovit</creatorcontrib><creatorcontrib>Wang, Yui-Hsi</creatorcontrib><title>ILC2s activated by IL-25 promote antigen-specific Th2 and Th9 functions that contribute to the control of Trichinella spiralis infection</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>IL-25, an IL-17 family cytokine, derived from epithelial cells was shown to regulate Th2- and Th9-type immune responses. We previously reported that IL-25 was important in promoting efficient protective immunity against T. spiralis infection; however, the cellular targets of IL-25 to elicit type-2 immunity during infection have not yet been addressed. Here, we investigated IL-25-responding cells and their involvement in mediating type-2 immune response during T. spiralis infection. ILC2 and CD4+ Th2 cells residing in the gastrointestinal tract of T. spiralis infected mice were found to express high levels of surface interleukin-17 receptor B (IL-17RB), a component of the IL-25 receptor. Following T. spiralis infection, activated ILC2s upregulated surface MHCII expression and enhanced capacity of effector T helper cell in producing antigen-specific Th2 and Th9 cytokines through MHCII-dependent interactions. Reciprocally, lack of CD4+ T helper cells impaired ILC2 function to produce type 2-associated cytokines in responding to IL-25 during T. spiralis infection. Furthermore, mice deficient in IL-17RB showed markedly reduced ILC2 numbers and antigen-specific Th2 and Th9 cytokine production during T. spiralis infection. The Il17rb-/- mice failed to mount effective antigen specific Th2 and Th9 functions resulting in diminished goblet cell and mast cell responses, leading to delayed worm expulsion in the intestines and muscles. 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metabolism</subject><subject>Interleukin-17 - metabolism</subject><subject>Interleukins</subject><subject>Intestine</subject><subject>Laboratory animals</subject><subject>Lymphocytes</subject><subject>Lymphocytes T</subject><subject>Mast Cells - immunology</subject><subject>Medical research</subject><subject>Medical technology</subject><subject>Medicine and Health Sciences</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Muscles</subject><subject>Physiological aspects</subject><subject>Receptors, Interleukin-17 - genetics</subject><subject>Receptors, Interleukin-17 - metabolism</subject><subject>Studies</subject><subject>T cells</subject><subject>Th2 Cells - immunology</subject><subject>Trichinella spiralis</subject><subject>Trichinella spiralis - immunology</subject><subject>Trichinellosis - immunology</subject><subject>Trichinosis</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNqNk12L1DAUhoso7rr6D0QDguhFxzRfbW6EZfBjYGBBR2_DaZpOM3SasUkX9x_4s013ustU9kJ6kXLyvG-SNzlJ8jLDi4zm2YedG_oO2sXBdWaBs4KJgj1KzjNJSSoIpo9P_s-SZ97vMOa0EOJpckaKQhakwOfJn9V6STwCHew1BFOh8gat1inh6NC7vQsGQRfs1nSpPxhta6vRpiGxWMVRonrootJ1HoUGAtKuC70thygLLpbMseJa5Gq06a1ubGfaFpA_2B5a65HtanPr8Dx5UkPrzYtpvEh-fP60WX5N11dfVsvLdaqFJCEtWQE1lLJmoEVJS8oMr5koRQaQl1pLrgnjkWAlz5iQoKWsSF5TmoOEjNOL5PXR99A6r6YQvYpRFRlhWMpIrI5E5WCnDr3dQ3-jHFh1W3D9VkEfrG6NEiXHNBek0hgzxgRUVaWLDERVMKaLOnp9nFYbyr2ptIlpQDsznc90tlFbd604l5zScbvvJoPe_RqMD2pvvR4z7IwbjvsWmBDJIvrmH_Th003UFuIBYvwurqtHU3XJMYuPQpA8UosHqPhVZm_jnZraxvpM8H4mGO_d_A5bGLxXq-_f_p-9-jln356wjYE2NN61w-2jm4PsCOreed-b-j7kDKuxYe7SUGPDqKlhouzV6QXdi-46hP4FI0IReg</recordid><startdate>20170912</startdate><enddate>20170912</enddate><creator>Angkasekwinai, Pornpimon</creator><creator>Sodthawon, Wichuda</creator><creator>Jeerawattanawart, Siranart</creator><creator>Hansakon, Adithap</creator><creator>Pattanapanyasat, Kovit</creator><creator>Wang, Yui-Hsi</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0003-0303-9544</orcidid></search><sort><creationdate>20170912</creationdate><title>ILC2s activated by IL-25 promote antigen-specific Th2 and Th9 functions that contribute to the control of Trichinella spiralis infection</title><author>Angkasekwinai, Pornpimon ; Sodthawon, Wichuda ; Jeerawattanawart, Siranart ; Hansakon, Adithap ; Pattanapanyasat, Kovit ; Wang, Yui-Hsi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-b48afab9f4ac6b3b34e5f46b61aa7bcc95c245fab4b51469ac99d27f337a9a153</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Animals</topic><topic>Antigens</topic><topic>Biology and Life Sciences</topic><topic>CD4 antigen</topic><topic>Cells, Cultured</topic><topic>Cloning</topic><topic>Cytokines</topic><topic>Development and progression</topic><topic>Epithelial cells</topic><topic>Expulsion</topic><topic>Gastrointestinal tract</topic><topic>Genes, MHC Class II</topic><topic>Genetic aspects</topic><topic>Goblet Cells - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Angkasekwinai, Pornpimon</au><au>Sodthawon, Wichuda</au><au>Jeerawattanawart, Siranart</au><au>Hansakon, Adithap</au><au>Pattanapanyasat, Kovit</au><au>Wang, Yui-Hsi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>ILC2s activated by IL-25 promote antigen-specific Th2 and Th9 functions that contribute to the control of Trichinella spiralis infection</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2017-09-12</date><risdate>2017</risdate><volume>12</volume><issue>9</issue><spage>e0184684</spage><epage>e0184684</epage><pages>e0184684-e0184684</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>IL-25, an IL-17 family cytokine, derived from epithelial cells was shown to regulate Th2- and Th9-type immune responses. We previously reported that IL-25 was important in promoting efficient protective immunity against T. spiralis infection; however, the cellular targets of IL-25 to elicit type-2 immunity during infection have not yet been addressed. Here, we investigated IL-25-responding cells and their involvement in mediating type-2 immune response during T. spiralis infection. ILC2 and CD4+ Th2 cells residing in the gastrointestinal tract of T. spiralis infected mice were found to express high levels of surface interleukin-17 receptor B (IL-17RB), a component of the IL-25 receptor. Following T. spiralis infection, activated ILC2s upregulated surface MHCII expression and enhanced capacity of effector T helper cell in producing antigen-specific Th2 and Th9 cytokines through MHCII-dependent interactions. Reciprocally, lack of CD4+ T helper cells impaired ILC2 function to produce type 2-associated cytokines in responding to IL-25 during T. spiralis infection. Furthermore, mice deficient in IL-17RB showed markedly reduced ILC2 numbers and antigen-specific Th2 and Th9 cytokine production during T. spiralis infection. The Il17rb-/- mice failed to mount effective antigen specific Th2 and Th9 functions resulting in diminished goblet cell and mast cell responses, leading to delayed worm expulsion in the intestines and muscles. Thus, our data indicated that ILC2s and CD4+ Th2 cells are the predominant cellular targets of IL-25 following T. spiralis infection and their collaborative interactions may play a key role in mounting effective antigen-specific Th2 and Th9 cytokine responses against T. spiralis infection.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>28898280</pmid><doi>10.1371/journal.pone.0184684</doi><tpages>e0184684</tpages><orcidid>https://orcid.org/0000-0003-0303-9544</orcidid><oa>free_for_read</oa></addata></record> |
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| recordid | cdi_plos_journals_1938124099 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Free Full-Text Journals in Chemistry; Public Library of Science (PLoS) |
| subjects | Animals Antigens Biology and Life Sciences CD4 antigen Cells, Cultured Cloning Cytokines Development and progression Epithelial cells Expulsion Gastrointestinal tract Genes, MHC Class II Genetic aspects Goblet Cells - immunology Health aspects Health sciences Helper cells Hospitals Immune response Immune system Immunity Immunity, Innate Immunology Infections Interleukin 1 Interleukin 17 Interleukin-10 - metabolism Interleukin-17 - metabolism Interleukins Intestine Laboratory animals Lymphocytes Lymphocytes T Mast Cells - immunology Medical research Medical technology Medicine and Health Sciences Mice Mice, Inbred BALB C Muscles Physiological aspects Receptors, Interleukin-17 - genetics Receptors, Interleukin-17 - metabolism Studies T cells Th2 Cells - immunology Trichinella spiralis Trichinella spiralis - immunology Trichinellosis - immunology Trichinosis |
| title | ILC2s activated by IL-25 promote antigen-specific Th2 and Th9 functions that contribute to the control of Trichinella spiralis infection |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-12T16%3A25%3A56IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=ILC2s%20activated%20by%20IL-25%20promote%20antigen-specific%20Th2%20and%20Th9%20functions%20that%20contribute%20to%20the%20control%20of%20Trichinella%20spiralis%20infection&rft.jtitle=PloS%20one&rft.au=Angkasekwinai,%20Pornpimon&rft.date=2017-09-12&rft.volume=12&rft.issue=9&rft.spage=e0184684&rft.epage=e0184684&rft.pages=e0184684-e0184684&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0184684&rft_dat=%3Cgale_plos_%3EA504280627%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1938124099&rft_id=info:pmid/28898280&rft_galeid=A504280627&rft_doaj_id=oai_doaj_org_article_6b503762dc004446adddc81a6d844c8f&rfr_iscdi=true |