Interferon-α exerts proinflammatory properties in experimental radiation-induced esophagitis: Possible involvement of plasmacytoid dendritic cells
Radiation-induced esophagitis, experienced during radiation therapy for lung cancer and head and neck cancer, is a major dose-limiting side effect of the treatment. This study aimed to elucidate the role of interferon-α (IFN-α) in radiation-induced esophagitis. C57BL/6 mice were exposed to 10 and 25...
Gespeichert in:
| Veröffentlicht in: | Life sciences (1973) 2022-01, Vol.289, p.120215-120215, Article 120215 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 120215 |
|---|---|
| container_issue | |
| container_start_page | 120215 |
| container_title | Life sciences (1973) |
| container_volume | 289 |
| creator | Kitamura, Hiroyuki Tanigawa, Tetsuya Kuzumoto, Takuya Nadatani, Yuji Otani, Koji Fukunaga, Shusei Hosomi, Shuhei Tanaka, Fumio Kamata, Noriko Nagami, Yasuaki Taira, Koichi Uematsu, Satoshi Watanabe, Toshio Fujiwara, Yasuhiro |
| description | Radiation-induced esophagitis, experienced during radiation therapy for lung cancer and head and neck cancer, is a major dose-limiting side effect of the treatment. This study aimed to elucidate the role of interferon-α (IFN-α) in radiation-induced esophagitis.
C57BL/6 mice were exposed to 10 and 25Gy of single thoracic irradiation. Esophageal mucosal damage and inflammatory reactions were assessed for 5 days after irradiation.
Irradiation induced esophagitis, characterized by reduction in the thickness of epithelial layer, upregulation of proinflammatory cytokines and chemokines, infiltration of inflammatory cells into the esophageal mucosa, and apoptosis of epithelial cells. Irradiation upregulated the level of gene expression for IFN-α in the esophageal tissue, and the neutralizing antibody against IFN-α ameliorated radiation-induced esophageal mucosal damage, while administration of IFN-α receptor agonist (RO8191) had an inverse effect. Depletion of plasmacytoid dendritic cells (pDCs) by anti-CD317 antibody or pharmacological inactivation with bortezomib suppressed radiation-induced mucosal inflammation and damage, accompanied by decrease in IFN-α expression level.
These findings suggest that IFN-α and pDCs exert proinflammatory properties in the pathophysiology of radiation-induced esophagitis.
•Irradiation to esophagus induce IFN-α in the esophageal mucosa.•IFN-α induce and promote inflammation in radiation-induced esophagitis.•Inhibition of IFN-α ameliorate radiation-induced esophagitis.•Depletion or inactivation of pDC reduce IFN-α in radiation-induced esophagitis.•Depletion or inactivation of pDC ameliorate radiation-induced esophagitis. |
| doi_str_mv | 10.1016/j.lfs.2021.120215 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2611663140</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0024320521012029</els_id><sourcerecordid>2611663140</sourcerecordid><originalsourceid>FETCH-LOGICAL-c424t-e3c3bbf2e441ec260ad5ab8a271f5ed549d7c09977ef9c938edb470fe10a1ddb3</originalsourceid><addsrcrecordid>eNp9kc-OFCEQxonRuOPqA3gxJF720rNA092DnjYb_2yyiR70TGgolAkNLdCTnefwSfZFfCbpzOrBgxdIpX5fper7EHpJyZYS2l_ut97mLSOMbun6do_Qhu4G0ZC-pY_RhhDGm5aR7gw9y3lPCOm6oX2Kzlq-E6QTZIN-3oQCyUKKofl1j-EOUsl4TtEF69U0qRLTca3n2nCQsQsVqoWbIBTlcVLGqeKq3AWzaDAYcpy_q2-uuPwGf445u9FD1R2iP8CqwtHi2as8KX0s0RlsIJhUeY01eJ-foydW-QwvHv5z9PX9uy_XH5vbTx9urq9uG80ZLw20uh1Hy4BzCpr1RJlOjTvFBmo7MB0XZtBEiGEAK7Rod2BGPhALlChqzNieo4vT3HrejwVykZPL6wYqQFyyZD2lfXWSk4q-_gfdxyWFul2lWMt7PoiVoidKp3p2Aivn6pNKR0mJXBOTe1kTk2tW8pRY1bx6mLyME5i_ij8RVeDtCYBqxcFBklk7CNVpl0AXaaL7z_jfomWr9g</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2623464790</pqid></control><display><type>article</type><title>Interferon-α exerts proinflammatory properties in experimental radiation-induced esophagitis: Possible involvement of plasmacytoid dendritic cells</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals</source><creator>Kitamura, Hiroyuki ; Tanigawa, Tetsuya ; Kuzumoto, Takuya ; Nadatani, Yuji ; Otani, Koji ; Fukunaga, Shusei ; Hosomi, Shuhei ; Tanaka, Fumio ; Kamata, Noriko ; Nagami, Yasuaki ; Taira, Koichi ; Uematsu, Satoshi ; Watanabe, Toshio ; Fujiwara, Yasuhiro</creator><creatorcontrib>Kitamura, Hiroyuki ; Tanigawa, Tetsuya ; Kuzumoto, Takuya ; Nadatani, Yuji ; Otani, Koji ; Fukunaga, Shusei ; Hosomi, Shuhei ; Tanaka, Fumio ; Kamata, Noriko ; Nagami, Yasuaki ; Taira, Koichi ; Uematsu, Satoshi ; Watanabe, Toshio ; Fujiwara, Yasuhiro</creatorcontrib><description>Radiation-induced esophagitis, experienced during radiation therapy for lung cancer and head and neck cancer, is a major dose-limiting side effect of the treatment. This study aimed to elucidate the role of interferon-α (IFN-α) in radiation-induced esophagitis.
C57BL/6 mice were exposed to 10 and 25Gy of single thoracic irradiation. Esophageal mucosal damage and inflammatory reactions were assessed for 5 days after irradiation.
Irradiation induced esophagitis, characterized by reduction in the thickness of epithelial layer, upregulation of proinflammatory cytokines and chemokines, infiltration of inflammatory cells into the esophageal mucosa, and apoptosis of epithelial cells. Irradiation upregulated the level of gene expression for IFN-α in the esophageal tissue, and the neutralizing antibody against IFN-α ameliorated radiation-induced esophageal mucosal damage, while administration of IFN-α receptor agonist (RO8191) had an inverse effect. Depletion of plasmacytoid dendritic cells (pDCs) by anti-CD317 antibody or pharmacological inactivation with bortezomib suppressed radiation-induced mucosal inflammation and damage, accompanied by decrease in IFN-α expression level.
These findings suggest that IFN-α and pDCs exert proinflammatory properties in the pathophysiology of radiation-induced esophagitis.
•Irradiation to esophagus induce IFN-α in the esophageal mucosa.•IFN-α induce and promote inflammation in radiation-induced esophagitis.•Inhibition of IFN-α ameliorate radiation-induced esophagitis.•Depletion or inactivation of pDC reduce IFN-α in radiation-induced esophagitis.•Depletion or inactivation of pDC ameliorate radiation-induced esophagitis.</description><identifier>ISSN: 0024-3205</identifier><identifier>EISSN: 1879-0631</identifier><identifier>DOI: 10.1016/j.lfs.2021.120215</identifier><identifier>PMID: 34890590</identifier><language>eng</language><publisher>Netherlands: Elsevier Inc</publisher><subject>Animals ; Antibodies ; Apoptosis ; Bortezomib ; Chemokines ; Cytokines ; Dendritic cells ; Dendritic Cells - immunology ; Depletion ; DNA damage ; Epithelial cells ; Epithelium ; Esophagitis ; Esophagitis - etiology ; Esophagitis - immunology ; Esophagus ; Gamma Rays - adverse effects ; Gene expression ; Head & neck cancer ; Inactivation ; Inflammation ; Interferon ; Interferon-alpha - immunology ; Interferon-α ; Irradiation ; Lung cancer ; Male ; Mice ; Mucosa ; Plasmacytoid dendritic cells ; Poly (ADP-ribose) polymerase ; Radiation ; Radiation damage ; Radiation effects ; Radiation Injuries, Experimental - immunology ; Radiation therapy ; Radiotherapy - adverse effects ; Thickness ; Thorax ; α-Interferon</subject><ispartof>Life sciences (1973), 2022-01, Vol.289, p.120215-120215, Article 120215</ispartof><rights>2021 Elsevier Inc.</rights><rights>Copyright © 2021 Elsevier Inc. All rights reserved.</rights><rights>Copyright Elsevier BV Jan 15, 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c424t-e3c3bbf2e441ec260ad5ab8a271f5ed549d7c09977ef9c938edb470fe10a1ddb3</citedby><cites>FETCH-LOGICAL-c424t-e3c3bbf2e441ec260ad5ab8a271f5ed549d7c09977ef9c938edb470fe10a1ddb3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.lfs.2021.120215$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,777,781,3537,27905,27906,45976</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34890590$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kitamura, Hiroyuki</creatorcontrib><creatorcontrib>Tanigawa, Tetsuya</creatorcontrib><creatorcontrib>Kuzumoto, Takuya</creatorcontrib><creatorcontrib>Nadatani, Yuji</creatorcontrib><creatorcontrib>Otani, Koji</creatorcontrib><creatorcontrib>Fukunaga, Shusei</creatorcontrib><creatorcontrib>Hosomi, Shuhei</creatorcontrib><creatorcontrib>Tanaka, Fumio</creatorcontrib><creatorcontrib>Kamata, Noriko</creatorcontrib><creatorcontrib>Nagami, Yasuaki</creatorcontrib><creatorcontrib>Taira, Koichi</creatorcontrib><creatorcontrib>Uematsu, Satoshi</creatorcontrib><creatorcontrib>Watanabe, Toshio</creatorcontrib><creatorcontrib>Fujiwara, Yasuhiro</creatorcontrib><title>Interferon-α exerts proinflammatory properties in experimental radiation-induced esophagitis: Possible involvement of plasmacytoid dendritic cells</title><title>Life sciences (1973)</title><addtitle>Life Sci</addtitle><description>Radiation-induced esophagitis, experienced during radiation therapy for lung cancer and head and neck cancer, is a major dose-limiting side effect of the treatment. This study aimed to elucidate the role of interferon-α (IFN-α) in radiation-induced esophagitis.
C57BL/6 mice were exposed to 10 and 25Gy of single thoracic irradiation. Esophageal mucosal damage and inflammatory reactions were assessed for 5 days after irradiation.
Irradiation induced esophagitis, characterized by reduction in the thickness of epithelial layer, upregulation of proinflammatory cytokines and chemokines, infiltration of inflammatory cells into the esophageal mucosa, and apoptosis of epithelial cells. Irradiation upregulated the level of gene expression for IFN-α in the esophageal tissue, and the neutralizing antibody against IFN-α ameliorated radiation-induced esophageal mucosal damage, while administration of IFN-α receptor agonist (RO8191) had an inverse effect. Depletion of plasmacytoid dendritic cells (pDCs) by anti-CD317 antibody or pharmacological inactivation with bortezomib suppressed radiation-induced mucosal inflammation and damage, accompanied by decrease in IFN-α expression level.
These findings suggest that IFN-α and pDCs exert proinflammatory properties in the pathophysiology of radiation-induced esophagitis.
•Irradiation to esophagus induce IFN-α in the esophageal mucosa.•IFN-α induce and promote inflammation in radiation-induced esophagitis.•Inhibition of IFN-α ameliorate radiation-induced esophagitis.•Depletion or inactivation of pDC reduce IFN-α in radiation-induced esophagitis.•Depletion or inactivation of pDC ameliorate radiation-induced esophagitis.</description><subject>Animals</subject><subject>Antibodies</subject><subject>Apoptosis</subject><subject>Bortezomib</subject><subject>Chemokines</subject><subject>Cytokines</subject><subject>Dendritic cells</subject><subject>Dendritic Cells - immunology</subject><subject>Depletion</subject><subject>DNA damage</subject><subject>Epithelial cells</subject><subject>Epithelium</subject><subject>Esophagitis</subject><subject>Esophagitis - etiology</subject><subject>Esophagitis - immunology</subject><subject>Esophagus</subject><subject>Gamma Rays - adverse effects</subject><subject>Gene expression</subject><subject>Head & neck cancer</subject><subject>Inactivation</subject><subject>Inflammation</subject><subject>Interferon</subject><subject>Interferon-alpha - immunology</subject><subject>Interferon-α</subject><subject>Irradiation</subject><subject>Lung cancer</subject><subject>Male</subject><subject>Mice</subject><subject>Mucosa</subject><subject>Plasmacytoid dendritic cells</subject><subject>Poly (ADP-ribose) polymerase</subject><subject>Radiation</subject><subject>Radiation damage</subject><subject>Radiation effects</subject><subject>Radiation Injuries, Experimental - immunology</subject><subject>Radiation therapy</subject><subject>Radiotherapy - adverse effects</subject><subject>Thickness</subject><subject>Thorax</subject><subject>α-Interferon</subject><issn>0024-3205</issn><issn>1879-0631</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kc-OFCEQxonRuOPqA3gxJF720rNA092DnjYb_2yyiR70TGgolAkNLdCTnefwSfZFfCbpzOrBgxdIpX5fper7EHpJyZYS2l_ut97mLSOMbun6do_Qhu4G0ZC-pY_RhhDGm5aR7gw9y3lPCOm6oX2Kzlq-E6QTZIN-3oQCyUKKofl1j-EOUsl4TtEF69U0qRLTca3n2nCQsQsVqoWbIBTlcVLGqeKq3AWzaDAYcpy_q2-uuPwGf445u9FD1R2iP8CqwtHi2as8KX0s0RlsIJhUeY01eJ-foydW-QwvHv5z9PX9uy_XH5vbTx9urq9uG80ZLw20uh1Hy4BzCpr1RJlOjTvFBmo7MB0XZtBEiGEAK7Rod2BGPhALlChqzNieo4vT3HrejwVykZPL6wYqQFyyZD2lfXWSk4q-_gfdxyWFul2lWMt7PoiVoidKp3p2Aivn6pNKR0mJXBOTe1kTk2tW8pRY1bx6mLyME5i_ij8RVeDtCYBqxcFBklk7CNVpl0AXaaL7z_jfomWr9g</recordid><startdate>20220115</startdate><enddate>20220115</enddate><creator>Kitamura, Hiroyuki</creator><creator>Tanigawa, Tetsuya</creator><creator>Kuzumoto, Takuya</creator><creator>Nadatani, Yuji</creator><creator>Otani, Koji</creator><creator>Fukunaga, Shusei</creator><creator>Hosomi, Shuhei</creator><creator>Tanaka, Fumio</creator><creator>Kamata, Noriko</creator><creator>Nagami, Yasuaki</creator><creator>Taira, Koichi</creator><creator>Uematsu, Satoshi</creator><creator>Watanabe, Toshio</creator><creator>Fujiwara, Yasuhiro</creator><general>Elsevier Inc</general><general>Elsevier BV</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>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20220115</creationdate><title>Interferon-α exerts proinflammatory properties in experimental radiation-induced esophagitis: Possible involvement of plasmacytoid dendritic cells</title><author>Kitamura, Hiroyuki ; Tanigawa, Tetsuya ; Kuzumoto, Takuya ; Nadatani, Yuji ; Otani, Koji ; Fukunaga, Shusei ; Hosomi, Shuhei ; Tanaka, Fumio ; Kamata, Noriko ; Nagami, Yasuaki ; Taira, Koichi ; Uematsu, Satoshi ; Watanabe, Toshio ; Fujiwara, Yasuhiro</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c424t-e3c3bbf2e441ec260ad5ab8a271f5ed549d7c09977ef9c938edb470fe10a1ddb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Animals</topic><topic>Antibodies</topic><topic>Apoptosis</topic><topic>Bortezomib</topic><topic>Chemokines</topic><topic>Cytokines</topic><topic>Dendritic cells</topic><topic>Dendritic Cells - immunology</topic><topic>Depletion</topic><topic>DNA damage</topic><topic>Epithelial cells</topic><topic>Epithelium</topic><topic>Esophagitis</topic><topic>Esophagitis - etiology</topic><topic>Esophagitis - immunology</topic><topic>Esophagus</topic><topic>Gamma Rays - adverse effects</topic><topic>Gene expression</topic><topic>Head & neck cancer</topic><topic>Inactivation</topic><topic>Inflammation</topic><topic>Interferon</topic><topic>Interferon-alpha - immunology</topic><topic>Interferon-α</topic><topic>Irradiation</topic><topic>Lung cancer</topic><topic>Male</topic><topic>Mice</topic><topic>Mucosa</topic><topic>Plasmacytoid dendritic cells</topic><topic>Poly (ADP-ribose) polymerase</topic><topic>Radiation</topic><topic>Radiation damage</topic><topic>Radiation effects</topic><topic>Radiation Injuries, Experimental - immunology</topic><topic>Radiation therapy</topic><topic>Radiotherapy - adverse effects</topic><topic>Thickness</topic><topic>Thorax</topic><topic>α-Interferon</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kitamura, Hiroyuki</creatorcontrib><creatorcontrib>Tanigawa, Tetsuya</creatorcontrib><creatorcontrib>Kuzumoto, Takuya</creatorcontrib><creatorcontrib>Nadatani, Yuji</creatorcontrib><creatorcontrib>Otani, Koji</creatorcontrib><creatorcontrib>Fukunaga, Shusei</creatorcontrib><creatorcontrib>Hosomi, Shuhei</creatorcontrib><creatorcontrib>Tanaka, Fumio</creatorcontrib><creatorcontrib>Kamata, Noriko</creatorcontrib><creatorcontrib>Nagami, Yasuaki</creatorcontrib><creatorcontrib>Taira, Koichi</creatorcontrib><creatorcontrib>Uematsu, Satoshi</creatorcontrib><creatorcontrib>Watanabe, Toshio</creatorcontrib><creatorcontrib>Fujiwara, Yasuhiro</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Life sciences (1973)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kitamura, Hiroyuki</au><au>Tanigawa, Tetsuya</au><au>Kuzumoto, Takuya</au><au>Nadatani, Yuji</au><au>Otani, Koji</au><au>Fukunaga, Shusei</au><au>Hosomi, Shuhei</au><au>Tanaka, Fumio</au><au>Kamata, Noriko</au><au>Nagami, Yasuaki</au><au>Taira, Koichi</au><au>Uematsu, Satoshi</au><au>Watanabe, Toshio</au><au>Fujiwara, Yasuhiro</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Interferon-α exerts proinflammatory properties in experimental radiation-induced esophagitis: Possible involvement of plasmacytoid dendritic cells</atitle><jtitle>Life sciences (1973)</jtitle><addtitle>Life Sci</addtitle><date>2022-01-15</date><risdate>2022</risdate><volume>289</volume><spage>120215</spage><epage>120215</epage><pages>120215-120215</pages><artnum>120215</artnum><issn>0024-3205</issn><eissn>1879-0631</eissn><abstract>Radiation-induced esophagitis, experienced during radiation therapy for lung cancer and head and neck cancer, is a major dose-limiting side effect of the treatment. This study aimed to elucidate the role of interferon-α (IFN-α) in radiation-induced esophagitis.
C57BL/6 mice were exposed to 10 and 25Gy of single thoracic irradiation. Esophageal mucosal damage and inflammatory reactions were assessed for 5 days after irradiation.
Irradiation induced esophagitis, characterized by reduction in the thickness of epithelial layer, upregulation of proinflammatory cytokines and chemokines, infiltration of inflammatory cells into the esophageal mucosa, and apoptosis of epithelial cells. Irradiation upregulated the level of gene expression for IFN-α in the esophageal tissue, and the neutralizing antibody against IFN-α ameliorated radiation-induced esophageal mucosal damage, while administration of IFN-α receptor agonist (RO8191) had an inverse effect. Depletion of plasmacytoid dendritic cells (pDCs) by anti-CD317 antibody or pharmacological inactivation with bortezomib suppressed radiation-induced mucosal inflammation and damage, accompanied by decrease in IFN-α expression level.
These findings suggest that IFN-α and pDCs exert proinflammatory properties in the pathophysiology of radiation-induced esophagitis.
•Irradiation to esophagus induce IFN-α in the esophageal mucosa.•IFN-α induce and promote inflammation in radiation-induced esophagitis.•Inhibition of IFN-α ameliorate radiation-induced esophagitis.•Depletion or inactivation of pDC reduce IFN-α in radiation-induced esophagitis.•Depletion or inactivation of pDC ameliorate radiation-induced esophagitis.</abstract><cop>Netherlands</cop><pub>Elsevier Inc</pub><pmid>34890590</pmid><doi>10.1016/j.lfs.2021.120215</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0024-3205 |
| ispartof | Life sciences (1973), 2022-01, Vol.289, p.120215-120215, Article 120215 |
| issn | 0024-3205 1879-0631 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_2611663140 |
| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | Animals Antibodies Apoptosis Bortezomib Chemokines Cytokines Dendritic cells Dendritic Cells - immunology Depletion DNA damage Epithelial cells Epithelium Esophagitis Esophagitis - etiology Esophagitis - immunology Esophagus Gamma Rays - adverse effects Gene expression Head & neck cancer Inactivation Inflammation Interferon Interferon-alpha - immunology Interferon-α Irradiation Lung cancer Male Mice Mucosa Plasmacytoid dendritic cells Poly (ADP-ribose) polymerase Radiation Radiation damage Radiation effects Radiation Injuries, Experimental - immunology Radiation therapy Radiotherapy - adverse effects Thickness Thorax α-Interferon |
| title | Interferon-α exerts proinflammatory properties in experimental radiation-induced esophagitis: Possible involvement of plasmacytoid dendritic cells |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-17T21%3A36%3A53IST&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=Interferon-%CE%B1%20exerts%20proinflammatory%20properties%20in%20experimental%20radiation-induced%20esophagitis:%20Possible%20involvement%20of%20plasmacytoid%20dendritic%20cells&rft.jtitle=Life%20sciences%20(1973)&rft.au=Kitamura,%20Hiroyuki&rft.date=2022-01-15&rft.volume=289&rft.spage=120215&rft.epage=120215&rft.pages=120215-120215&rft.artnum=120215&rft.issn=0024-3205&rft.eissn=1879-0631&rft_id=info:doi/10.1016/j.lfs.2021.120215&rft_dat=%3Cproquest_cross%3E2611663140%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=2623464790&rft_id=info:pmid/34890590&rft_els_id=S0024320521012029&rfr_iscdi=true |