M2 macrophage immunotherapy abolishes glucose intolerance by increasing IL-10 expression and AKT activation
Glucose intolerance associates with M1/M2 macrophage unbalance. We thus wanted to examine the effect of M2 macrophage administration on mouse model of glucose intolerance. C57BL/6 mice fed a high-fat diet (HFD) for 12 weeks and then received thrice 20 mg/kg streptozotocin (HFD-GI). Bone marrow-deriv...
Gespeichert in:
| Veröffentlicht in: | Immunotherapy 2020-01, Vol.12 (1), p.9-24 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 24 |
|---|---|
| container_issue | 1 |
| container_start_page | 9 |
| container_title | Immunotherapy |
| container_volume | 12 |
| creator | Vega-Galaviz, Diana Vecchyo-Tenorio, Georgina Del Alcántara-Suárez, Raúl Méndez-García, Lucia A Sánchez-Del Real, Ana L Villalobos-Molina, Rafael Fragoso, José M León-Cabrera, Sonia Ostoa-Saloma, Pedro Pérez-Tamayo, Ruy Escobedo, Galileo |
| description | Glucose intolerance associates with M1/M2 macrophage unbalance. We thus wanted to examine the effect of M2 macrophage administration on mouse model of glucose intolerance.
C57BL/6 mice fed a high-fat diet (HFD) for 12 weeks and then received thrice 20 mg/kg streptozotocin (HFD-GI). Bone marrow-derived stem cells were collected from donor mice and differentiated/activated into M2 macrophages for intraperitoneal administration into HFD-GI mice.
M2 macrophage treatment abolished glucose intolerance independently of obesity. M2 macrophage administration increased IL-10 in visceral adipose tissue and serum, but showed no effect on serum insulin. While nitric oxide synthase-2 and arginase-1 remained unaltered, M2 macrophage treatment restored AKT phosphorylation in visceral adipose tissue.
M2 macrophage treatment abolishes glucose intolerance by increasing IL-10 and phosphorylated AKT. |
| doi_str_mv | 10.2217/imt-2019-0080 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_journals_2501456930</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2501456930</sourcerecordid><originalsourceid>FETCH-LOGICAL-c437t-24b112e0efaed3eb8925075f3ceb079539ddda95ef457c9fe5ad9a6ab8d3a8663</originalsourceid><addsrcrecordid>eNp1kD1PwzAQhi0EoqUwsiJLzAE7dj48VhUfFUUsRWKzHOfSujROsBNE_z2uUrox2ed7_J7uQeiakrs4ptm9qbsoJlREhOTkBI1plpAo4zw_Pd7ZxwhdeL8hJOVZys_RiFFBeR7nY_T5GuNaade0a7UCbOq6t023BqfaHVZFszV-DR6vtr1ufOjbrtmGptWAi10otQPljV3h-SKiBMNP68B701isbImnL0usdGe-VReeLtFZpbYerg7nBL0_Pixnz9Hi7Wk-my4izVkWtuEFpTEQqBSUDIpcxAnJkoppKEgmEibKslQigYonmRYVJKoUKlVFXjKVpymboNsht3XNVw--k5umdzaMlCGJ8iQVjAQqGqiwvPcOKtk6Uyu3k5TIvVoZ1Mq9WrlXG_ibQ2pf1FAe6T-XARADUPVdHyxoA0GTHKrww2hj4Z_wX0tfick</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2501456930</pqid></control><display><type>article</type><title>M2 macrophage immunotherapy abolishes glucose intolerance by increasing IL-10 expression and AKT activation</title><source>MEDLINE</source><source>PubMed Central</source><creator>Vega-Galaviz, Diana ; Vecchyo-Tenorio, Georgina Del ; Alcántara-Suárez, Raúl ; Méndez-García, Lucia A ; Sánchez-Del Real, Ana L ; Villalobos-Molina, Rafael ; Fragoso, José M ; León-Cabrera, Sonia ; Ostoa-Saloma, Pedro ; Pérez-Tamayo, Ruy ; Escobedo, Galileo</creator><creatorcontrib>Vega-Galaviz, Diana ; Vecchyo-Tenorio, Georgina Del ; Alcántara-Suárez, Raúl ; Méndez-García, Lucia A ; Sánchez-Del Real, Ana L ; Villalobos-Molina, Rafael ; Fragoso, José M ; León-Cabrera, Sonia ; Ostoa-Saloma, Pedro ; Pérez-Tamayo, Ruy ; Escobedo, Galileo</creatorcontrib><description>Glucose intolerance associates with M1/M2 macrophage unbalance. We thus wanted to examine the effect of M2 macrophage administration on mouse model of glucose intolerance.
C57BL/6 mice fed a high-fat diet (HFD) for 12 weeks and then received thrice 20 mg/kg streptozotocin (HFD-GI). Bone marrow-derived stem cells were collected from donor mice and differentiated/activated into M2 macrophages for intraperitoneal administration into HFD-GI mice.
M2 macrophage treatment abolished glucose intolerance independently of obesity. M2 macrophage administration increased IL-10 in visceral adipose tissue and serum, but showed no effect on serum insulin. While nitric oxide synthase-2 and arginase-1 remained unaltered, M2 macrophage treatment restored AKT phosphorylation in visceral adipose tissue.
M2 macrophage treatment abolishes glucose intolerance by increasing IL-10 and phosphorylated AKT.</description><identifier>ISSN: 1750-743X</identifier><identifier>EISSN: 1750-7448</identifier><identifier>DOI: 10.2217/imt-2019-0080</identifier><identifier>PMID: 31914828</identifier><language>eng</language><publisher>England: Future Medicine Ltd</publisher><subject>Adipose tissue ; AKT ; AKT protein ; Animals ; Antibodies ; Arg-1 ; Arginase ; Bone marrow ; Chromium ; Diabetes Mellitus, Type 2 - immunology ; Diabetes Mellitus, Type 2 - therapy ; Diet ; Diet, High-Fat ; Disease Models, Animal ; Glucose ; Glucose Intolerance ; Glucose tolerance ; High fat diet ; Humans ; IL-10 ; Immunotherapy ; Immunotherapy - methods ; Insulin ; Insulin Resistance ; Interleukin 10 ; Interleukin-10 - genetics ; Interleukin-10 - metabolism ; Intolerance ; Kinases ; Lipoproteins ; macrophage ; Macrophages ; Macrophages - immunology ; Male ; Mice ; Mice, Inbred C57BL ; Nitric oxide ; Nitric-oxide synthase ; NOS-2 ; Obesity ; Phosphorylation ; Proto-Oncogene Proteins c-akt - metabolism ; Signal Transduction ; Stem cell transplantation ; Stem cells ; Streptozocin ; streptozotocin ; Th2 Cells - immunology ; Triglycerides ; Type 2 diabetes ; visceral adipose tissue</subject><ispartof>Immunotherapy, 2020-01, Vol.12 (1), p.9-24</ispartof><rights>2020 Future Medicine Ltd</rights><rights>Copyright Future Medicine Ltd Jan 2020</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c437t-24b112e0efaed3eb8925075f3ceb079539ddda95ef457c9fe5ad9a6ab8d3a8663</citedby><cites>FETCH-LOGICAL-c437t-24b112e0efaed3eb8925075f3ceb079539ddda95ef457c9fe5ad9a6ab8d3a8663</cites><orcidid>0000-0002-9224-7400</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31914828$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Vega-Galaviz, Diana</creatorcontrib><creatorcontrib>Vecchyo-Tenorio, Georgina Del</creatorcontrib><creatorcontrib>Alcántara-Suárez, Raúl</creatorcontrib><creatorcontrib>Méndez-García, Lucia A</creatorcontrib><creatorcontrib>Sánchez-Del Real, Ana L</creatorcontrib><creatorcontrib>Villalobos-Molina, Rafael</creatorcontrib><creatorcontrib>Fragoso, José M</creatorcontrib><creatorcontrib>León-Cabrera, Sonia</creatorcontrib><creatorcontrib>Ostoa-Saloma, Pedro</creatorcontrib><creatorcontrib>Pérez-Tamayo, Ruy</creatorcontrib><creatorcontrib>Escobedo, Galileo</creatorcontrib><title>M2 macrophage immunotherapy abolishes glucose intolerance by increasing IL-10 expression and AKT activation</title><title>Immunotherapy</title><addtitle>Immunotherapy</addtitle><description>Glucose intolerance associates with M1/M2 macrophage unbalance. We thus wanted to examine the effect of M2 macrophage administration on mouse model of glucose intolerance.
C57BL/6 mice fed a high-fat diet (HFD) for 12 weeks and then received thrice 20 mg/kg streptozotocin (HFD-GI). Bone marrow-derived stem cells were collected from donor mice and differentiated/activated into M2 macrophages for intraperitoneal administration into HFD-GI mice.
M2 macrophage treatment abolished glucose intolerance independently of obesity. M2 macrophage administration increased IL-10 in visceral adipose tissue and serum, but showed no effect on serum insulin. While nitric oxide synthase-2 and arginase-1 remained unaltered, M2 macrophage treatment restored AKT phosphorylation in visceral adipose tissue.
M2 macrophage treatment abolishes glucose intolerance by increasing IL-10 and phosphorylated AKT.</description><subject>Adipose tissue</subject><subject>AKT</subject><subject>AKT protein</subject><subject>Animals</subject><subject>Antibodies</subject><subject>Arg-1</subject><subject>Arginase</subject><subject>Bone marrow</subject><subject>Chromium</subject><subject>Diabetes Mellitus, Type 2 - immunology</subject><subject>Diabetes Mellitus, Type 2 - therapy</subject><subject>Diet</subject><subject>Diet, High-Fat</subject><subject>Disease Models, Animal</subject><subject>Glucose</subject><subject>Glucose Intolerance</subject><subject>Glucose tolerance</subject><subject>High fat diet</subject><subject>Humans</subject><subject>IL-10</subject><subject>Immunotherapy</subject><subject>Immunotherapy - methods</subject><subject>Insulin</subject><subject>Insulin Resistance</subject><subject>Interleukin 10</subject><subject>Interleukin-10 - genetics</subject><subject>Interleukin-10 - metabolism</subject><subject>Intolerance</subject><subject>Kinases</subject><subject>Lipoproteins</subject><subject>macrophage</subject><subject>Macrophages</subject><subject>Macrophages - immunology</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Nitric oxide</subject><subject>Nitric-oxide synthase</subject><subject>NOS-2</subject><subject>Obesity</subject><subject>Phosphorylation</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Signal Transduction</subject><subject>Stem cell transplantation</subject><subject>Stem cells</subject><subject>Streptozocin</subject><subject>streptozotocin</subject><subject>Th2 Cells - immunology</subject><subject>Triglycerides</subject><subject>Type 2 diabetes</subject><subject>visceral adipose tissue</subject><issn>1750-743X</issn><issn>1750-7448</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>eNp1kD1PwzAQhi0EoqUwsiJLzAE7dj48VhUfFUUsRWKzHOfSujROsBNE_z2uUrox2ed7_J7uQeiakrs4ptm9qbsoJlREhOTkBI1plpAo4zw_Pd7ZxwhdeL8hJOVZys_RiFFBeR7nY_T5GuNaade0a7UCbOq6t023BqfaHVZFszV-DR6vtr1ufOjbrtmGptWAi10otQPljV3h-SKiBMNP68B701isbImnL0usdGe-VReeLtFZpbYerg7nBL0_Pixnz9Hi7Wk-my4izVkWtuEFpTEQqBSUDIpcxAnJkoppKEgmEibKslQigYonmRYVJKoUKlVFXjKVpymboNsht3XNVw--k5umdzaMlCGJ8iQVjAQqGqiwvPcOKtk6Uyu3k5TIvVoZ1Mq9WrlXG_ibQ2pf1FAe6T-XARADUPVdHyxoA0GTHKrww2hj4Z_wX0tfick</recordid><startdate>20200101</startdate><enddate>20200101</enddate><creator>Vega-Galaviz, Diana</creator><creator>Vecchyo-Tenorio, Georgina Del</creator><creator>Alcántara-Suárez, Raúl</creator><creator>Méndez-García, Lucia A</creator><creator>Sánchez-Del Real, Ana L</creator><creator>Villalobos-Molina, Rafael</creator><creator>Fragoso, José M</creator><creator>León-Cabrera, Sonia</creator><creator>Ostoa-Saloma, Pedro</creator><creator>Pérez-Tamayo, Ruy</creator><creator>Escobedo, Galileo</creator><general>Future Medicine Ltd</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>8AO</scope><scope>8C1</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>EHMNL</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><orcidid>https://orcid.org/0000-0002-9224-7400</orcidid></search><sort><creationdate>20200101</creationdate><title>M2 macrophage immunotherapy abolishes glucose intolerance by increasing IL-10 expression and AKT activation</title><author>Vega-Galaviz, Diana ; Vecchyo-Tenorio, Georgina Del ; Alcántara-Suárez, Raúl ; Méndez-García, Lucia A ; Sánchez-Del Real, Ana L ; Villalobos-Molina, Rafael ; Fragoso, José M ; León-Cabrera, Sonia ; Ostoa-Saloma, Pedro ; Pérez-Tamayo, Ruy ; Escobedo, Galileo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c437t-24b112e0efaed3eb8925075f3ceb079539ddda95ef457c9fe5ad9a6ab8d3a8663</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Adipose tissue</topic><topic>AKT</topic><topic>AKT protein</topic><topic>Animals</topic><topic>Antibodies</topic><topic>Arg-1</topic><topic>Arginase</topic><topic>Bone marrow</topic><topic>Chromium</topic><topic>Diabetes Mellitus, Type 2 - immunology</topic><topic>Diabetes Mellitus, Type 2 - therapy</topic><topic>Diet</topic><topic>Diet, High-Fat</topic><topic>Disease Models, Animal</topic><topic>Glucose</topic><topic>Glucose Intolerance</topic><topic>Glucose tolerance</topic><topic>High fat diet</topic><topic>Humans</topic><topic>IL-10</topic><topic>Immunotherapy</topic><topic>Immunotherapy - methods</topic><topic>Insulin</topic><topic>Insulin Resistance</topic><topic>Interleukin 10</topic><topic>Interleukin-10 - genetics</topic><topic>Interleukin-10 - metabolism</topic><topic>Intolerance</topic><topic>Kinases</topic><topic>Lipoproteins</topic><topic>macrophage</topic><topic>Macrophages</topic><topic>Macrophages - immunology</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Nitric oxide</topic><topic>Nitric-oxide synthase</topic><topic>NOS-2</topic><topic>Obesity</topic><topic>Phosphorylation</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Signal Transduction</topic><topic>Stem cell transplantation</topic><topic>Stem cells</topic><topic>Streptozocin</topic><topic>streptozotocin</topic><topic>Th2 Cells - immunology</topic><topic>Triglycerides</topic><topic>Type 2 diabetes</topic><topic>visceral adipose tissue</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Vega-Galaviz, Diana</creatorcontrib><creatorcontrib>Vecchyo-Tenorio, Georgina Del</creatorcontrib><creatorcontrib>Alcántara-Suárez, Raúl</creatorcontrib><creatorcontrib>Méndez-García, Lucia A</creatorcontrib><creatorcontrib>Sánchez-Del Real, Ana L</creatorcontrib><creatorcontrib>Villalobos-Molina, Rafael</creatorcontrib><creatorcontrib>Fragoso, José M</creatorcontrib><creatorcontrib>León-Cabrera, Sonia</creatorcontrib><creatorcontrib>Ostoa-Saloma, Pedro</creatorcontrib><creatorcontrib>Pérez-Tamayo, Ruy</creatorcontrib><creatorcontrib>Escobedo, Galileo</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 Pharma Collection</collection><collection>Public Health Database</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>UK & Ireland Database</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><jtitle>Immunotherapy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Vega-Galaviz, Diana</au><au>Vecchyo-Tenorio, Georgina Del</au><au>Alcántara-Suárez, Raúl</au><au>Méndez-García, Lucia A</au><au>Sánchez-Del Real, Ana L</au><au>Villalobos-Molina, Rafael</au><au>Fragoso, José M</au><au>León-Cabrera, Sonia</au><au>Ostoa-Saloma, Pedro</au><au>Pérez-Tamayo, Ruy</au><au>Escobedo, Galileo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>M2 macrophage immunotherapy abolishes glucose intolerance by increasing IL-10 expression and AKT activation</atitle><jtitle>Immunotherapy</jtitle><addtitle>Immunotherapy</addtitle><date>2020-01-01</date><risdate>2020</risdate><volume>12</volume><issue>1</issue><spage>9</spage><epage>24</epage><pages>9-24</pages><issn>1750-743X</issn><eissn>1750-7448</eissn><abstract>Glucose intolerance associates with M1/M2 macrophage unbalance. We thus wanted to examine the effect of M2 macrophage administration on mouse model of glucose intolerance.
C57BL/6 mice fed a high-fat diet (HFD) for 12 weeks and then received thrice 20 mg/kg streptozotocin (HFD-GI). Bone marrow-derived stem cells were collected from donor mice and differentiated/activated into M2 macrophages for intraperitoneal administration into HFD-GI mice.
M2 macrophage treatment abolished glucose intolerance independently of obesity. M2 macrophage administration increased IL-10 in visceral adipose tissue and serum, but showed no effect on serum insulin. While nitric oxide synthase-2 and arginase-1 remained unaltered, M2 macrophage treatment restored AKT phosphorylation in visceral adipose tissue.
M2 macrophage treatment abolishes glucose intolerance by increasing IL-10 and phosphorylated AKT.</abstract><cop>England</cop><pub>Future Medicine Ltd</pub><pmid>31914828</pmid><doi>10.2217/imt-2019-0080</doi><tpages>16</tpages><orcidid>https://orcid.org/0000-0002-9224-7400</orcidid></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1750-743X |
| ispartof | Immunotherapy, 2020-01, Vol.12 (1), p.9-24 |
| issn | 1750-743X 1750-7448 |
| language | eng |
| recordid | cdi_proquest_journals_2501456930 |
| source | MEDLINE; PubMed Central |
| subjects | Adipose tissue AKT AKT protein Animals Antibodies Arg-1 Arginase Bone marrow Chromium Diabetes Mellitus, Type 2 - immunology Diabetes Mellitus, Type 2 - therapy Diet Diet, High-Fat Disease Models, Animal Glucose Glucose Intolerance Glucose tolerance High fat diet Humans IL-10 Immunotherapy Immunotherapy - methods Insulin Insulin Resistance Interleukin 10 Interleukin-10 - genetics Interleukin-10 - metabolism Intolerance Kinases Lipoproteins macrophage Macrophages Macrophages - immunology Male Mice Mice, Inbred C57BL Nitric oxide Nitric-oxide synthase NOS-2 Obesity Phosphorylation Proto-Oncogene Proteins c-akt - metabolism Signal Transduction Stem cell transplantation Stem cells Streptozocin streptozotocin Th2 Cells - immunology Triglycerides Type 2 diabetes visceral adipose tissue |
| title | M2 macrophage immunotherapy abolishes glucose intolerance by increasing IL-10 expression and AKT activation |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-26T23%3A55%3A58IST&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=M2%20macrophage%20immunotherapy%20abolishes%20glucose%20intolerance%20by%20increasing%20IL-10%20expression%20and%20AKT%20activation&rft.jtitle=Immunotherapy&rft.au=Vega-Galaviz,%20Diana&rft.date=2020-01-01&rft.volume=12&rft.issue=1&rft.spage=9&rft.epage=24&rft.pages=9-24&rft.issn=1750-743X&rft.eissn=1750-7448&rft_id=info:doi/10.2217/imt-2019-0080&rft_dat=%3Cproquest_cross%3E2501456930%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=2501456930&rft_id=info:pmid/31914828&rfr_iscdi=true |