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Myeloid-derived suppressor cells regulate the immunosuppressive functions of PD-1−PD-L1+ Bregs through PD-L1/PI3K/AKT/NF-κB axis in breast cancer
Myeloid-derived suppressor cells (MDSCs) are a heterogeneous group of myeloid cells that are closely related to tumor immune escape, but the mechanism by which MDSCs regulate B cells has not been elucidated. Our previous studies revealed that breast cancer-derived MDSCs could induce a group of PD-1...
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| Published in: | Cell death & disease 2021-05, Vol.12 (5), p.465-465, Article 465 |
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| container_end_page | 465 |
| container_issue | 5 |
| container_start_page | 465 |
| container_title | Cell death & disease |
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| creator | Liu, Min Wei, Feng Wang, Jian Yu, Wenwen Shen, Meng Liu, Ting Zhang, Dong Wang, Yang Ren, Xiubao Sun, Qian |
| description | Myeloid-derived suppressor cells (MDSCs) are a heterogeneous group of myeloid cells that are closely related to tumor immune escape, but the mechanism by which MDSCs regulate B cells has not been elucidated. Our previous studies revealed that breast cancer-derived MDSCs could induce a group of PD-1
−
PD-L1
+
Bregs with immunosuppressive functions. Here, we reported that blocking PD-1/PD-L1 interaction between MDSCs and B cells could reverse the immunosuppressive functions of PD-1
−
PD-L1
+
Bregs. The activation of PI3K/AKT/NF-κB signaling pathway is essential for PD-1
−
PD-L1
+
Bregs to exert immunosuppressive effects. MDSCs activated the PI3K/AKT/NF-κB pathway in B cells via the PD-1/PD-L1 axis. Furthermore, inhibition of PD-1/PD-L1 or PI3K/AKT signaling suppressed both tumor growth and the immunosuppressive functions of PD-1
−
PD-L1
+
Bregs. Dual suppression of PD-1/PD-L1 and PI3K/AKT exerted better antitumor effect. Finally, MDSCs and PD-1
−
PD-L1
+
Bregs were colocalized in breast cancer tissues and PD-1
−
PD-L1
+
Bregs were positively correlated with poor prognosis. Thus, MDSC-educated PD-1
−
PD-L1
+
Bregs and their regulatory mechanisms could contribute to the immunosuppressive tumor microenvironment. Our study proposes a novel mechanism for MDSC-mediated regulation of B cell immunity, which might shed new light on tumor immunotherapy.
+ |
| doi_str_mv | 10.1038/s41419-021-03745-1 |
| format | article |
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−
PD-L1
+
Bregs with immunosuppressive functions. Here, we reported that blocking PD-1/PD-L1 interaction between MDSCs and B cells could reverse the immunosuppressive functions of PD-1
−
PD-L1
+
Bregs. The activation of PI3K/AKT/NF-κB signaling pathway is essential for PD-1
−
PD-L1
+
Bregs to exert immunosuppressive effects. MDSCs activated the PI3K/AKT/NF-κB pathway in B cells via the PD-1/PD-L1 axis. Furthermore, inhibition of PD-1/PD-L1 or PI3K/AKT signaling suppressed both tumor growth and the immunosuppressive functions of PD-1
−
PD-L1
+
Bregs. Dual suppression of PD-1/PD-L1 and PI3K/AKT exerted better antitumor effect. Finally, MDSCs and PD-1
−
PD-L1
+
Bregs were colocalized in breast cancer tissues and PD-1
−
PD-L1
+
Bregs were positively correlated with poor prognosis. Thus, MDSC-educated PD-1
−
PD-L1
+
Bregs and their regulatory mechanisms could contribute to the immunosuppressive tumor microenvironment. Our study proposes a novel mechanism for MDSC-mediated regulation of B cell immunity, which might shed new light on tumor immunotherapy.
+</description><identifier>ISSN: 2041-4889</identifier><identifier>EISSN: 2041-4889</identifier><identifier>DOI: 10.1038/s41419-021-03745-1</identifier><identifier>PMID: 33967272</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>1-Phosphatidylinositol 3-kinase ; 13/1 ; 13/109 ; 13/31 ; 13/51 ; 13/89 ; 13/95 ; 14/28 ; 64/60 ; 692/699/67/1347 ; 692/699/67/327 ; AKT protein ; Antibodies ; Antitumor activity ; Biochemistry ; Biomedical and Life Sciences ; Breast cancer ; Cell Biology ; Cell Culture ; Immunology ; Immunotherapy ; Life Sciences ; Lymphocytes B ; Myeloid cells ; NF-κB protein ; PD-1 protein ; PD-L1 protein ; Signal transduction ; Suppressor cells ; Tumor microenvironment</subject><ispartof>Cell death & disease, 2021-05, Vol.12 (5), p.465-465, Article 465</ispartof><rights>The Author(s) 2021</rights><rights>The Author(s) 2021. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c470t-de624421700cd706166396dc63f0e9684c7dbca8d8a03cd0bcf3308965100c583</citedby><cites>FETCH-LOGICAL-c470t-de624421700cd706166396dc63f0e9684c7dbca8d8a03cd0bcf3308965100c583</cites><orcidid>0000-0002-4878-3599</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2524031161/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2524031161?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793,75126</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33967272$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Min</creatorcontrib><creatorcontrib>Wei, Feng</creatorcontrib><creatorcontrib>Wang, Jian</creatorcontrib><creatorcontrib>Yu, Wenwen</creatorcontrib><creatorcontrib>Shen, Meng</creatorcontrib><creatorcontrib>Liu, Ting</creatorcontrib><creatorcontrib>Zhang, Dong</creatorcontrib><creatorcontrib>Wang, Yang</creatorcontrib><creatorcontrib>Ren, Xiubao</creatorcontrib><creatorcontrib>Sun, Qian</creatorcontrib><title>Myeloid-derived suppressor cells regulate the immunosuppressive functions of PD-1−PD-L1+ Bregs through PD-L1/PI3K/AKT/NF-κB axis in breast cancer</title><title>Cell death & disease</title><addtitle>Cell Death Dis</addtitle><addtitle>Cell Death Dis</addtitle><description>Myeloid-derived suppressor cells (MDSCs) are a heterogeneous group of myeloid cells that are closely related to tumor immune escape, but the mechanism by which MDSCs regulate B cells has not been elucidated. Our previous studies revealed that breast cancer-derived MDSCs could induce a group of PD-1
−
PD-L1
+
Bregs with immunosuppressive functions. Here, we reported that blocking PD-1/PD-L1 interaction between MDSCs and B cells could reverse the immunosuppressive functions of PD-1
−
PD-L1
+
Bregs. The activation of PI3K/AKT/NF-κB signaling pathway is essential for PD-1
−
PD-L1
+
Bregs to exert immunosuppressive effects. MDSCs activated the PI3K/AKT/NF-κB pathway in B cells via the PD-1/PD-L1 axis. Furthermore, inhibition of PD-1/PD-L1 or PI3K/AKT signaling suppressed both tumor growth and the immunosuppressive functions of PD-1
−
PD-L1
+
Bregs. Dual suppression of PD-1/PD-L1 and PI3K/AKT exerted better antitumor effect. Finally, MDSCs and PD-1
−
PD-L1
+
Bregs were colocalized in breast cancer tissues and PD-1
−
PD-L1
+
Bregs were positively correlated with poor prognosis. Thus, MDSC-educated PD-1
−
PD-L1
+
Bregs and their regulatory mechanisms could contribute to the immunosuppressive tumor microenvironment. Our study proposes a novel mechanism for MDSC-mediated regulation of B cell immunity, which might shed new light on tumor immunotherapy.
+</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>13/1</subject><subject>13/109</subject><subject>13/31</subject><subject>13/51</subject><subject>13/89</subject><subject>13/95</subject><subject>14/28</subject><subject>64/60</subject><subject>692/699/67/1347</subject><subject>692/699/67/327</subject><subject>AKT protein</subject><subject>Antibodies</subject><subject>Antitumor activity</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Breast cancer</subject><subject>Cell Biology</subject><subject>Cell Culture</subject><subject>Immunology</subject><subject>Immunotherapy</subject><subject>Life Sciences</subject><subject>Lymphocytes B</subject><subject>Myeloid cells</subject><subject>NF-κB protein</subject><subject>PD-1 protein</subject><subject>PD-L1 protein</subject><subject>Signal transduction</subject><subject>Suppressor cells</subject><subject>Tumor microenvironment</subject><issn>2041-4889</issn><issn>2041-4889</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNp9UktuFDEQbSEQiUIuwAJZYoOEmvGvbfcGKQkERhkgi7C23LZ7xqNue7C7I3ID1ojTcAgOwUnwTCchYYE3ZVW996rKfkXxFMFXCBIxSxRRVJcQoxISTqsSPSj2MaSopELUD-_c94rDlNYwH0IgrtjjYo-QmnHM8X7x48OV7YIzpbHRXVoD0rjZRJtSiEDbrksg2uXYqcGCYWWB6_vRhxtMJoB29HpwwScQWnD-pkS_v33PYYFeguNMTZkWw7hcgV1ydj4nZ7Ojs4vZx9Py189joL66BJwHTbQqDUArr218UjxqVZfs4XU8KD6fvr04eV8uPr2bnxwtSk05HPLIDFOKEYdQGw4ZYizvZTQjLbQ1E1Rz02gljFCQaAMb3eYXEDWrUGZUghwU80nXBLWWm-h6Fa9kUE7uEiEupYqD052VbVMzRGkOFNKaq6ZuMYbcVDo3qhqatV5PWpux6a3R1g9RdfdE71e8W8lluJQCQY54nQVeXAvE8GW0aZC9S9svUN6GMUlcYSpyLwEz9Pk_0HUYo89PtUNBghBDGYUnlI4hpWjb22EQlFsPyclDMntI7jwkt6Rnd9e4pdw4JgPIBEi55Jc2_u39H9k_7L7SLg</recordid><startdate>20210509</startdate><enddate>20210509</enddate><creator>Liu, Min</creator><creator>Wei, Feng</creator><creator>Wang, Jian</creator><creator>Yu, Wenwen</creator><creator>Shen, Meng</creator><creator>Liu, Ting</creator><creator>Zhang, Dong</creator><creator>Wang, Yang</creator><creator>Ren, Xiubao</creator><creator>Sun, Qian</creator><general>Nature Publishing Group UK</general><general>Springer Nature B.V</general><general>Nature Publishing Group</general><scope>C6C</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88I</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>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M2P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0002-4878-3599</orcidid></search><sort><creationdate>20210509</creationdate><title>Myeloid-derived suppressor cells regulate the immunosuppressive functions of PD-1−PD-L1+ Bregs through PD-L1/PI3K/AKT/NF-κB axis in breast cancer</title><author>Liu, Min ; Wei, Feng ; Wang, Jian ; Yu, Wenwen ; Shen, Meng ; Liu, Ting ; Zhang, Dong ; Wang, Yang ; Ren, Xiubao ; Sun, Qian</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c470t-de624421700cd706166396dc63f0e9684c7dbca8d8a03cd0bcf3308965100c583</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>13/1</topic><topic>13/109</topic><topic>13/31</topic><topic>13/51</topic><topic>13/89</topic><topic>13/95</topic><topic>14/28</topic><topic>64/60</topic><topic>692/699/67/1347</topic><topic>692/699/67/327</topic><topic>AKT protein</topic><topic>Antibodies</topic><topic>Antitumor activity</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Breast cancer</topic><topic>Cell Biology</topic><topic>Cell Culture</topic><topic>Immunology</topic><topic>Immunotherapy</topic><topic>Life Sciences</topic><topic>Lymphocytes B</topic><topic>Myeloid cells</topic><topic>NF-κB protein</topic><topic>PD-1 protein</topic><topic>PD-L1 protein</topic><topic>Signal transduction</topic><topic>Suppressor cells</topic><topic>Tumor microenvironment</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Min</creatorcontrib><creatorcontrib>Wei, Feng</creatorcontrib><creatorcontrib>Wang, Jian</creatorcontrib><creatorcontrib>Yu, Wenwen</creatorcontrib><creatorcontrib>Shen, Meng</creatorcontrib><creatorcontrib>Liu, Ting</creatorcontrib><creatorcontrib>Zhang, Dong</creatorcontrib><creatorcontrib>Wang, Yang</creatorcontrib><creatorcontrib>Ren, Xiubao</creatorcontrib><creatorcontrib>Sun, Qian</creatorcontrib><collection>Springer_OA刊</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Science 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)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>ProQuest 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>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>Science Database</collection><collection>ProQuest Biological Science Journals</collection><collection>ProQuest - Publicly Available Content 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>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>Directory of Open Access Journals(OpenAccess)</collection><jtitle>Cell death & disease</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Min</au><au>Wei, Feng</au><au>Wang, Jian</au><au>Yu, Wenwen</au><au>Shen, Meng</au><au>Liu, Ting</au><au>Zhang, Dong</au><au>Wang, Yang</au><au>Ren, Xiubao</au><au>Sun, Qian</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Myeloid-derived suppressor cells regulate the immunosuppressive functions of PD-1−PD-L1+ Bregs through PD-L1/PI3K/AKT/NF-κB axis in breast cancer</atitle><jtitle>Cell death & disease</jtitle><stitle>Cell Death Dis</stitle><addtitle>Cell Death Dis</addtitle><date>2021-05-09</date><risdate>2021</risdate><volume>12</volume><issue>5</issue><spage>465</spage><epage>465</epage><pages>465-465</pages><artnum>465</artnum><issn>2041-4889</issn><eissn>2041-4889</eissn><abstract>Myeloid-derived suppressor cells (MDSCs) are a heterogeneous group of myeloid cells that are closely related to tumor immune escape, but the mechanism by which MDSCs regulate B cells has not been elucidated. Our previous studies revealed that breast cancer-derived MDSCs could induce a group of PD-1
−
PD-L1
+
Bregs with immunosuppressive functions. Here, we reported that blocking PD-1/PD-L1 interaction between MDSCs and B cells could reverse the immunosuppressive functions of PD-1
−
PD-L1
+
Bregs. The activation of PI3K/AKT/NF-κB signaling pathway is essential for PD-1
−
PD-L1
+
Bregs to exert immunosuppressive effects. MDSCs activated the PI3K/AKT/NF-κB pathway in B cells via the PD-1/PD-L1 axis. Furthermore, inhibition of PD-1/PD-L1 or PI3K/AKT signaling suppressed both tumor growth and the immunosuppressive functions of PD-1
−
PD-L1
+
Bregs. Dual suppression of PD-1/PD-L1 and PI3K/AKT exerted better antitumor effect. Finally, MDSCs and PD-1
−
PD-L1
+
Bregs were colocalized in breast cancer tissues and PD-1
−
PD-L1
+
Bregs were positively correlated with poor prognosis. Thus, MDSC-educated PD-1
−
PD-L1
+
Bregs and their regulatory mechanisms could contribute to the immunosuppressive tumor microenvironment. Our study proposes a novel mechanism for MDSC-mediated regulation of B cell immunity, which might shed new light on tumor immunotherapy.
+</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>33967272</pmid><doi>10.1038/s41419-021-03745-1</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0002-4878-3599</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 2041-4889 |
| ispartof | Cell death & disease, 2021-05, Vol.12 (5), p.465-465, Article 465 |
| issn | 2041-4889 2041-4889 |
| language | eng |
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| source | PubMed Central(OpenAccess); ProQuest - Publicly Available Content Database; Springer Nature - nature.com Journals - Fully Open Access |
| subjects | 1-Phosphatidylinositol 3-kinase 13/1 13/109 13/31 13/51 13/89 13/95 14/28 64/60 692/699/67/1347 692/699/67/327 AKT protein Antibodies Antitumor activity Biochemistry Biomedical and Life Sciences Breast cancer Cell Biology Cell Culture Immunology Immunotherapy Life Sciences Lymphocytes B Myeloid cells NF-κB protein PD-1 protein PD-L1 protein Signal transduction Suppressor cells Tumor microenvironment |
| title | Myeloid-derived suppressor cells regulate the immunosuppressive functions of PD-1−PD-L1+ Bregs through PD-L1/PI3K/AKT/NF-κB axis in breast cancer |
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