MicroRNA-219a-5p suppresses intestinal inflammation through inhibiting Th1/Th17-mediated immune responses in inflammatory bowel disease
MicroRNA (miR)-219a-5p has been implicated in the development of numerous progression of carcinoma and autoimmune diseases. However, whether miR-219a-5p is involved in the pathogenesis of inflammatory bowel disease (IBD) remains elusive. In this study, we demonstrated that miR-219a-5p expression was...
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| Veröffentlicht in: | Mucosal immunology 2020-03, Vol.13 (2), p.303-312 |
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| creator | Shi, Yan Dai, Shenglan Qiu, Caiyu Wang, Tao Zhou, Yong Xue, Cuihua Yao, Jun Xu, Yaping |
| description | MicroRNA (miR)-219a-5p has been implicated in the development of numerous progression of carcinoma and autoimmune diseases. However, whether miR-219a-5p is involved in the pathogenesis of inflammatory bowel disease (IBD) remains elusive. In this study, we demonstrated that miR-219a-5p expression was significantly decreased in the inflamed intestinal mucosa and peripheral blood (PB)-CD4
+
T cells from patients with IBD. Proinflammatory cytokines (e.g., IL-6, IL-12, IL-23 and TNF-α) inhibited miR-219a-5p expression in CD4
+
T cells in vitro. Lentivirus-mediated miR-219a-5p downregulation facilitated Th1/Th17 cell differentiation, whereas miR-219a-5p overexpression exerted an opposite effect. Luciferase assays confirmed that ETS variant 5 (ETV5) was a functional target of miR-219a-5p and ETV5 expression was significantly increased in the inflamed intestinal mucosa and PB-CD4
+
T cells from IBD patients. ETV5 overexpression enhanced Th1/Th17 immune response through upregulating the phosphorylation of STAT3 and STAT4. Importantly, supplementation of miR-219a-5p ameliorated TNBS-induced intestinal mucosal inflammation, characterized by decreased IFN-γ
+
CD4
+
T cells and IL-17A
+
CD4
+
T cells infiltration in the colonic lamina propria. Our data thus reveal a novel mechanism whereby miR-219a-5p suppresses intestinal inflammation through inhibiting Th1/Th17-mediated immune responses. miR-219a-5p might be a target for the treatment of IBD. |
| doi_str_mv | 10.1038/s41385-019-0216-7 |
| format | Article |
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+
T cells from patients with IBD. Proinflammatory cytokines (e.g., IL-6, IL-12, IL-23 and TNF-α) inhibited miR-219a-5p expression in CD4
+
T cells in vitro. Lentivirus-mediated miR-219a-5p downregulation facilitated Th1/Th17 cell differentiation, whereas miR-219a-5p overexpression exerted an opposite effect. Luciferase assays confirmed that ETS variant 5 (ETV5) was a functional target of miR-219a-5p and ETV5 expression was significantly increased in the inflamed intestinal mucosa and PB-CD4
+
T cells from IBD patients. ETV5 overexpression enhanced Th1/Th17 immune response through upregulating the phosphorylation of STAT3 and STAT4. Importantly, supplementation of miR-219a-5p ameliorated TNBS-induced intestinal mucosal inflammation, characterized by decreased IFN-γ
+
CD4
+
T cells and IL-17A
+
CD4
+
T cells infiltration in the colonic lamina propria. Our data thus reveal a novel mechanism whereby miR-219a-5p suppresses intestinal inflammation through inhibiting Th1/Th17-mediated immune responses. miR-219a-5p might be a target for the treatment of IBD.</description><identifier>ISSN: 1933-0219</identifier><identifier>EISSN: 1935-3456</identifier><identifier>DOI: 10.1038/s41385-019-0216-7</identifier><identifier>PMID: 31628427</identifier><language>eng</language><publisher>New York: Nature Publishing Group US</publisher><subject>Adult ; Allergology ; Animals ; Antibodies ; Autoimmune diseases ; Biomedical and Life Sciences ; Biomedicine ; CD4 antigen ; Cell differentiation ; Cells, Cultured ; Colitis - genetics ; Colitis - immunology ; Colon ; Disease Models, Animal ; DNA-Binding Proteins - genetics ; DNA-Binding Proteins - metabolism ; Female ; Gastroenterology ; Gene Expression Regulation ; Helper cells ; Humans ; Immunology ; Inflammation ; Inflammatory bowel disease ; Inflammatory bowel diseases ; Inflammatory Bowel Diseases - genetics ; Inflammatory Bowel Diseases - immunology ; Interleukin 12 ; Interleukin 23 ; Interleukin 6 ; Intestine ; Lamina propria ; Lymphocytes ; Lymphocytes T ; Male ; Mice ; Mice, Inbred BALB C ; MicroRNAs ; MicroRNAs - genetics ; Middle Aged ; miRNA ; Mucosa ; Peripheral blood ; Phosphorylation ; Stat3 protein ; Stat4 protein ; Supplements ; Th1 Cells - immunology ; Th17 Cells - immunology ; Transcription Factors - genetics ; Transcription Factors - metabolism ; Trinitrobenzenesulfonic Acid ; Tumor necrosis factor-α ; γ-Interferon</subject><ispartof>Mucosal immunology, 2020-03, Vol.13 (2), p.303-312</ispartof><rights>Society for Mucosal Immunology 2019</rights><rights>2019© Society for Mucosal Immunology 2019</rights><rights>Society for Mucosal Immunology 2019.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c443t-8732cde23a8ca21e9f1c53d323b50c374da2d95f35636d9631804907f26127c3</citedby><cites>FETCH-LOGICAL-c443t-8732cde23a8ca21e9f1c53d323b50c374da2d95f35636d9631804907f26127c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.proquest.com/docview/2362206623?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,64385,64387,64389,72469</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31628427$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shi, Yan</creatorcontrib><creatorcontrib>Dai, Shenglan</creatorcontrib><creatorcontrib>Qiu, Caiyu</creatorcontrib><creatorcontrib>Wang, Tao</creatorcontrib><creatorcontrib>Zhou, Yong</creatorcontrib><creatorcontrib>Xue, Cuihua</creatorcontrib><creatorcontrib>Yao, Jun</creatorcontrib><creatorcontrib>Xu, Yaping</creatorcontrib><title>MicroRNA-219a-5p suppresses intestinal inflammation through inhibiting Th1/Th17-mediated immune responses in inflammatory bowel disease</title><title>Mucosal immunology</title><addtitle>Mucosal Immunol</addtitle><addtitle>Mucosal Immunol</addtitle><description>MicroRNA (miR)-219a-5p has been implicated in the development of numerous progression of carcinoma and autoimmune diseases. However, whether miR-219a-5p is involved in the pathogenesis of inflammatory bowel disease (IBD) remains elusive. In this study, we demonstrated that miR-219a-5p expression was significantly decreased in the inflamed intestinal mucosa and peripheral blood (PB)-CD4
+
T cells from patients with IBD. Proinflammatory cytokines (e.g., IL-6, IL-12, IL-23 and TNF-α) inhibited miR-219a-5p expression in CD4
+
T cells in vitro. Lentivirus-mediated miR-219a-5p downregulation facilitated Th1/Th17 cell differentiation, whereas miR-219a-5p overexpression exerted an opposite effect. Luciferase assays confirmed that ETS variant 5 (ETV5) was a functional target of miR-219a-5p and ETV5 expression was significantly increased in the inflamed intestinal mucosa and PB-CD4
+
T cells from IBD patients. ETV5 overexpression enhanced Th1/Th17 immune response through upregulating the phosphorylation of STAT3 and STAT4. Importantly, supplementation of miR-219a-5p ameliorated TNBS-induced intestinal mucosal inflammation, characterized by decreased IFN-γ
+
CD4
+
T cells and IL-17A
+
CD4
+
T cells infiltration in the colonic lamina propria. Our data thus reveal a novel mechanism whereby miR-219a-5p suppresses intestinal inflammation through inhibiting Th1/Th17-mediated immune responses. miR-219a-5p might be a target for the treatment of IBD.</description><subject>Adult</subject><subject>Allergology</subject><subject>Animals</subject><subject>Antibodies</subject><subject>Autoimmune diseases</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>CD4 antigen</subject><subject>Cell differentiation</subject><subject>Cells, Cultured</subject><subject>Colitis - genetics</subject><subject>Colitis - immunology</subject><subject>Colon</subject><subject>Disease Models, Animal</subject><subject>DNA-Binding Proteins - genetics</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>Female</subject><subject>Gastroenterology</subject><subject>Gene Expression Regulation</subject><subject>Helper cells</subject><subject>Humans</subject><subject>Immunology</subject><subject>Inflammation</subject><subject>Inflammatory bowel disease</subject><subject>Inflammatory bowel diseases</subject><subject>Inflammatory Bowel Diseases - genetics</subject><subject>Inflammatory Bowel Diseases - immunology</subject><subject>Interleukin 12</subject><subject>Interleukin 23</subject><subject>Interleukin 6</subject><subject>Intestine</subject><subject>Lamina propria</subject><subject>Lymphocytes</subject><subject>Lymphocytes T</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>MicroRNAs</subject><subject>MicroRNAs - genetics</subject><subject>Middle Aged</subject><subject>miRNA</subject><subject>Mucosa</subject><subject>Peripheral blood</subject><subject>Phosphorylation</subject><subject>Stat3 protein</subject><subject>Stat4 protein</subject><subject>Supplements</subject><subject>Th1 Cells - immunology</subject><subject>Th17 Cells - immunology</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - metabolism</subject><subject>Trinitrobenzenesulfonic Acid</subject><subject>Tumor necrosis factor-α</subject><subject>γ-Interferon</subject><issn>1933-0219</issn><issn>1935-3456</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</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>eNp9kc1O3TAQha2KCijwAN1UkdiwcbE9_kmWCFFaCYqE7t7yTZx7jZI4tRMhnoDX7twGilSpLCyPPN-ckc8h5DNnXzmD8jxLDqWijFeUCa6p-UAOeQWKglR6708Nu051QD7l_MCYZkzBPjkArkUphTkkz7ehTvH-5wVFzFE1Fnkex-Rz9rkIw-TzFAbXYdl2ru_dFOJQTNsU580WH7dhHRDYFKstP8djaO-b4CbfFKHv58EXKDXGYVF7U4npqVjHR98VTcjeZX9MPrauy_7k5T4iq29Xq8vv9Obu-sflxQ2tpYSJlgZE3XgBrqyd4L5qea2gAQFrxWowsnGiqVQLSoNuKg28ZLJiphWaC1PDETlbZMcUf834OduHXPuuc4OPc7YCmOGyLLVG9PQf9CHOCb1AShqFXnL-PgVaCKa1AKT4QqHXOSff2jGF3qUny5ndRWmXKC1GaXdRWoMzX16U5zWa-nfiNTsExAJkbA0bn95W_1_1N5fNqGE</recordid><startdate>20200301</startdate><enddate>20200301</enddate><creator>Shi, Yan</creator><creator>Dai, Shenglan</creator><creator>Qiu, Caiyu</creator><creator>Wang, Tao</creator><creator>Zhou, Yong</creator><creator>Xue, Cuihua</creator><creator>Yao, Jun</creator><creator>Xu, Yaping</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>20200301</creationdate><title>MicroRNA-219a-5p suppresses intestinal inflammation through inhibiting Th1/Th17-mediated immune responses in inflammatory bowel disease</title><author>Shi, Yan ; Dai, Shenglan ; Qiu, Caiyu ; Wang, Tao ; Zhou, Yong ; Xue, Cuihua ; Yao, Jun ; Xu, Yaping</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c443t-8732cde23a8ca21e9f1c53d323b50c374da2d95f35636d9631804907f26127c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Adult</topic><topic>Allergology</topic><topic>Animals</topic><topic>Antibodies</topic><topic>Autoimmune diseases</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>CD4 antigen</topic><topic>Cell differentiation</topic><topic>Cells, Cultured</topic><topic>Colitis - genetics</topic><topic>Colitis - immunology</topic><topic>Colon</topic><topic>Disease Models, Animal</topic><topic>DNA-Binding Proteins - genetics</topic><topic>DNA-Binding Proteins - metabolism</topic><topic>Female</topic><topic>Gastroenterology</topic><topic>Gene Expression Regulation</topic><topic>Helper cells</topic><topic>Humans</topic><topic>Immunology</topic><topic>Inflammation</topic><topic>Inflammatory bowel disease</topic><topic>Inflammatory bowel diseases</topic><topic>Inflammatory Bowel Diseases - genetics</topic><topic>Inflammatory Bowel Diseases - immunology</topic><topic>Interleukin 12</topic><topic>Interleukin 23</topic><topic>Interleukin 6</topic><topic>Intestine</topic><topic>Lamina propria</topic><topic>Lymphocytes</topic><topic>Lymphocytes T</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>MicroRNAs</topic><topic>MicroRNAs - genetics</topic><topic>Middle Aged</topic><topic>miRNA</topic><topic>Mucosa</topic><topic>Peripheral blood</topic><topic>Phosphorylation</topic><topic>Stat3 protein</topic><topic>Stat4 protein</topic><topic>Supplements</topic><topic>Th1 Cells - immunology</topic><topic>Th17 Cells - immunology</topic><topic>Transcription Factors - genetics</topic><topic>Transcription Factors - metabolism</topic><topic>Trinitrobenzenesulfonic Acid</topic><topic>Tumor necrosis factor-α</topic><topic>γ-Interferon</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shi, Yan</creatorcontrib><creatorcontrib>Dai, Shenglan</creatorcontrib><creatorcontrib>Qiu, Caiyu</creatorcontrib><creatorcontrib>Wang, Tao</creatorcontrib><creatorcontrib>Zhou, Yong</creatorcontrib><creatorcontrib>Xue, Cuihua</creatorcontrib><creatorcontrib>Yao, Jun</creatorcontrib><creatorcontrib>Xu, Yaping</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>Shi, Yan</au><au>Dai, Shenglan</au><au>Qiu, Caiyu</au><au>Wang, Tao</au><au>Zhou, Yong</au><au>Xue, Cuihua</au><au>Yao, Jun</au><au>Xu, Yaping</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MicroRNA-219a-5p suppresses intestinal inflammation through inhibiting Th1/Th17-mediated immune responses in inflammatory bowel disease</atitle><jtitle>Mucosal immunology</jtitle><stitle>Mucosal Immunol</stitle><addtitle>Mucosal Immunol</addtitle><date>2020-03-01</date><risdate>2020</risdate><volume>13</volume><issue>2</issue><spage>303</spage><epage>312</epage><pages>303-312</pages><issn>1933-0219</issn><eissn>1935-3456</eissn><abstract>MicroRNA (miR)-219a-5p has been implicated in the development of numerous progression of carcinoma and autoimmune diseases. However, whether miR-219a-5p is involved in the pathogenesis of inflammatory bowel disease (IBD) remains elusive. In this study, we demonstrated that miR-219a-5p expression was significantly decreased in the inflamed intestinal mucosa and peripheral blood (PB)-CD4
+
T cells from patients with IBD. Proinflammatory cytokines (e.g., IL-6, IL-12, IL-23 and TNF-α) inhibited miR-219a-5p expression in CD4
+
T cells in vitro. Lentivirus-mediated miR-219a-5p downregulation facilitated Th1/Th17 cell differentiation, whereas miR-219a-5p overexpression exerted an opposite effect. Luciferase assays confirmed that ETS variant 5 (ETV5) was a functional target of miR-219a-5p and ETV5 expression was significantly increased in the inflamed intestinal mucosa and PB-CD4
+
T cells from IBD patients. ETV5 overexpression enhanced Th1/Th17 immune response through upregulating the phosphorylation of STAT3 and STAT4. Importantly, supplementation of miR-219a-5p ameliorated TNBS-induced intestinal mucosal inflammation, characterized by decreased IFN-γ
+
CD4
+
T cells and IL-17A
+
CD4
+
T cells infiltration in the colonic lamina propria. Our data thus reveal a novel mechanism whereby miR-219a-5p suppresses intestinal inflammation through inhibiting Th1/Th17-mediated immune responses. miR-219a-5p might be a target for the treatment of IBD.</abstract><cop>New York</cop><pub>Nature Publishing Group US</pub><pmid>31628427</pmid><doi>10.1038/s41385-019-0216-7</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Mucosal immunology, 2020-03, Vol.13 (2), p.303-312 |
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| language | eng |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; ProQuest Central UK/Ireland; Alma/SFX Local Collection |
| subjects | Adult Allergology Animals Antibodies Autoimmune diseases Biomedical and Life Sciences Biomedicine CD4 antigen Cell differentiation Cells, Cultured Colitis - genetics Colitis - immunology Colon Disease Models, Animal DNA-Binding Proteins - genetics DNA-Binding Proteins - metabolism Female Gastroenterology Gene Expression Regulation Helper cells Humans Immunology Inflammation Inflammatory bowel disease Inflammatory bowel diseases Inflammatory Bowel Diseases - genetics Inflammatory Bowel Diseases - immunology Interleukin 12 Interleukin 23 Interleukin 6 Intestine Lamina propria Lymphocytes Lymphocytes T Male Mice Mice, Inbred BALB C MicroRNAs MicroRNAs - genetics Middle Aged miRNA Mucosa Peripheral blood Phosphorylation Stat3 protein Stat4 protein Supplements Th1 Cells - immunology Th17 Cells - immunology Transcription Factors - genetics Transcription Factors - metabolism Trinitrobenzenesulfonic Acid Tumor necrosis factor-α γ-Interferon |
| title | MicroRNA-219a-5p suppresses intestinal inflammation through inhibiting Th1/Th17-mediated immune responses in inflammatory bowel disease |
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