CD14+ CD15− HLA-DR− myeloid-derived suppressor cells impair antimicrobial responses in patients with acute-on-chronic liver failure
ObjectiveImmune paresis in patients with acute-on-chronic liver failure (ACLF) accounts for infection susceptibility and increased mortality. Immunosuppressive mononuclear CD14+HLA-DR− myeloid-derived suppressor cells (M-MDSCs) have recently been identified to quell antimicrobial responses in immune...
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| Veröffentlicht in: | Gut 2018-06, Vol.67 (6), p.1155-1167 |
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| creator | Bernsmeier, Christine Triantafyllou, Evangelos Brenig, Robert Lebosse, Fanny J Singanayagam, Arjuna Patel, Vishal C Pop, Oltin T Khamri, Wafa Nathwani, Rooshi Tidswell, Robert Weston, Christopher J Adams, David H Thursz, Mark R Wendon, Julia A Antoniades, Charalambos Gustav |
| description | ObjectiveImmune paresis in patients with acute-on-chronic liver failure (ACLF) accounts for infection susceptibility and increased mortality. Immunosuppressive mononuclear CD14+HLA-DR− myeloid-derived suppressor cells (M-MDSCs) have recently been identified to quell antimicrobial responses in immune-mediated diseases. We sought to delineate the function and derivation of M-MDSC in patients with ACLF, and explore potential targets to augment antimicrobial responses.DesignPatients with ACLF (n=41) were compared with healthy subjects (n=25) and patients with cirrhosis (n=22) or acute liver failure (n=30). CD14+CD15−CD11b+HLA-DR− cells were identified as per definition of M-MDSC and detailed immunophenotypic analyses were performed. Suppression of T cell activation was assessed by mixed lymphocyte reaction. Assessment of innate immune function included cytokine expression in response to Toll-like receptor (TLR-2, TLR-4 and TLR-9) stimulation and phagocytosis assays using flow cytometry and live cell imaging-based techniques.ResultsCirculating CD14+CD15−CD11b+HLA-DR− M-MDSCs were markedly expanded in patients with ACLF (55% of CD14+ cells). M-MDSC displayed immunosuppressive properties, significantly decreasing T cell proliferation (p=0.01), producing less tumour necrosis factor-alpha/interleukin-6 in response to TLR stimulation (all p |
| doi_str_mv | 10.1136/gutjnl-2017-314184 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5969362</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1907325360</sourcerecordid><originalsourceid>FETCH-LOGICAL-b474t-a2052cc97337adfd6cb4cdd0af199b4b9c3d9c6556df6d5d10f25665cba5f15d3</originalsourceid><addsrcrecordid>eNqNkc2KFDEUhYMozjj6Ai4kS0Wi-a_KRmh61BYaBNF1SCWp6TRVlTKp6mGeQNc-ok9iihoHdeUmCTnfPTe5B4CnBL8ihMnXV_N0HDpEMakQI5zU_B44J1zWiNG6vg_O8aKIiqsz8CjnI8a4rhV5CM5oLRTlrD4H37aXhL-EZRU_v_-Au_0GXX5aTv2N72JwyPkUTt7BPI9j8jnHBK3vugxDP5qQoBmm0AebYhNMBwsxxiH7Ig9wNFPww5ThdZgO0Nh58igOyB5SHIKFXfFNsDWhm5N_DB60psv-ye1-Ab68e_t5u0P7j-8_bDd71PCKT8hQLKi1qmKsMq510jbcOodNS5RqeKMsc8pKIaRrpROO4JYKKYVtjGiJcOwCvFl9x7npvbPlfcl0ekyhN-lGRxP038oQDvoqnrRQUjFJi8GL1eDwT9lus9fLHeZEsKpWJ1LY57fNUvw6-zzpPuRlembwcc6aKFwxKpjEBaUrWiaZc_LtnTfBeklbr2nrJW29pl2Knv35mbuS3_EWAK1A0x__x_AXV7259Q</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1907325360</pqid></control><display><type>article</type><title>CD14+ CD15− HLA-DR− myeloid-derived suppressor cells impair antimicrobial responses in patients with acute-on-chronic liver failure</title><source>MEDLINE</source><source>PubMed Central</source><creator>Bernsmeier, Christine ; Triantafyllou, Evangelos ; Brenig, Robert ; Lebosse, Fanny J ; Singanayagam, Arjuna ; Patel, Vishal C ; Pop, Oltin T ; Khamri, Wafa ; Nathwani, Rooshi ; Tidswell, Robert ; Weston, Christopher J ; Adams, David H ; Thursz, Mark R ; Wendon, Julia A ; Antoniades, Charalambos Gustav</creator><creatorcontrib>Bernsmeier, Christine ; Triantafyllou, Evangelos ; Brenig, Robert ; Lebosse, Fanny J ; Singanayagam, Arjuna ; Patel, Vishal C ; Pop, Oltin T ; Khamri, Wafa ; Nathwani, Rooshi ; Tidswell, Robert ; Weston, Christopher J ; Adams, David H ; Thursz, Mark R ; Wendon, Julia A ; Antoniades, Charalambos Gustav</creatorcontrib><description>ObjectiveImmune paresis in patients with acute-on-chronic liver failure (ACLF) accounts for infection susceptibility and increased mortality. Immunosuppressive mononuclear CD14+HLA-DR− myeloid-derived suppressor cells (M-MDSCs) have recently been identified to quell antimicrobial responses in immune-mediated diseases. We sought to delineate the function and derivation of M-MDSC in patients with ACLF, and explore potential targets to augment antimicrobial responses.DesignPatients with ACLF (n=41) were compared with healthy subjects (n=25) and patients with cirrhosis (n=22) or acute liver failure (n=30). CD14+CD15−CD11b+HLA-DR− cells were identified as per definition of M-MDSC and detailed immunophenotypic analyses were performed. Suppression of T cell activation was assessed by mixed lymphocyte reaction. Assessment of innate immune function included cytokine expression in response to Toll-like receptor (TLR-2, TLR-4 and TLR-9) stimulation and phagocytosis assays using flow cytometry and live cell imaging-based techniques.ResultsCirculating CD14+CD15−CD11b+HLA-DR− M-MDSCs were markedly expanded in patients with ACLF (55% of CD14+ cells). M-MDSC displayed immunosuppressive properties, significantly decreasing T cell proliferation (p=0.01), producing less tumour necrosis factor-alpha/interleukin-6 in response to TLR stimulation (all p<0.01), and reduced bacterial uptake of Escherichia coli (p<0.001). Persistently low expression of HLA-DR during disease evolution was linked to secondary infection and 28-day mortality. Recurrent TLR-2 and TLR-4 stimulation expanded M-MDSC in vitro. By contrast, TLR-3 agonism reconstituted HLA-DR expression and innate immune function ex vivo.ConclusionImmunosuppressive CD14+HLA-DR− M-MDSCs are expanded in patients with ACLF. They were depicted by suppressing T cell function, attenuated antimicrobial innate immune responses, linked to secondary infection, disease severity and prognosis. TLR-3 agonism reversed M-MDSC expansion and innate immune function and merits further evaluation as potential immunotherapeutic agent.</description><identifier>ISSN: 0017-5749</identifier><identifier>EISSN: 1468-3288</identifier><identifier>DOI: 10.1136/gutjnl-2017-314184</identifier><identifier>PMID: 28592438</identifier><language>eng</language><publisher>England: BMJ Publishing Group</publisher><subject>Acute-On-Chronic Liver Failure - immunology ; Adult ; Anti-Infective Agents - therapeutic use ; Cytokines - metabolism ; Flow Cytometry ; Fucosyltransferases - metabolism ; Hepatology ; HLA-DR Antigens - metabolism ; Humans ; Immune Tolerance - immunology ; Immunology ; Immunophenotyping ; Lewis X Antigen - metabolism ; Life Sciences ; Lipopolysaccharide Receptors - metabolism ; Lymphocyte Activation - immunology ; Middle Aged ; Myeloid-Derived Suppressor Cells - immunology ; Phagocytosis - immunology ; Polymerase Chain Reaction ; Prognosis</subject><ispartof>Gut, 2018-06, Vol.67 (6), p.1155-1167</ispartof><rights>Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2018. All rights reserved. No commercial use is permitted unless otherwise expressly granted.</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><rights>Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2018. All rights reserved. No commercial use is permitted unless otherwise expressly granted. 2018</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b474t-a2052cc97337adfd6cb4cdd0af199b4b9c3d9c6556df6d5d10f25665cba5f15d3</citedby><cites>FETCH-LOGICAL-b474t-a2052cc97337adfd6cb4cdd0af199b4b9c3d9c6556df6d5d10f25665cba5f15d3</cites><orcidid>0000-0002-3411-1580</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/PMC5969362/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5969362/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28592438$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-04153789$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Bernsmeier, Christine</creatorcontrib><creatorcontrib>Triantafyllou, Evangelos</creatorcontrib><creatorcontrib>Brenig, Robert</creatorcontrib><creatorcontrib>Lebosse, Fanny J</creatorcontrib><creatorcontrib>Singanayagam, Arjuna</creatorcontrib><creatorcontrib>Patel, Vishal C</creatorcontrib><creatorcontrib>Pop, Oltin T</creatorcontrib><creatorcontrib>Khamri, Wafa</creatorcontrib><creatorcontrib>Nathwani, Rooshi</creatorcontrib><creatorcontrib>Tidswell, Robert</creatorcontrib><creatorcontrib>Weston, Christopher J</creatorcontrib><creatorcontrib>Adams, David H</creatorcontrib><creatorcontrib>Thursz, Mark R</creatorcontrib><creatorcontrib>Wendon, Julia A</creatorcontrib><creatorcontrib>Antoniades, Charalambos Gustav</creatorcontrib><title>CD14+ CD15− HLA-DR− myeloid-derived suppressor cells impair antimicrobial responses in patients with acute-on-chronic liver failure</title><title>Gut</title><addtitle>Gut</addtitle><description>ObjectiveImmune paresis in patients with acute-on-chronic liver failure (ACLF) accounts for infection susceptibility and increased mortality. Immunosuppressive mononuclear CD14+HLA-DR− myeloid-derived suppressor cells (M-MDSCs) have recently been identified to quell antimicrobial responses in immune-mediated diseases. We sought to delineate the function and derivation of M-MDSC in patients with ACLF, and explore potential targets to augment antimicrobial responses.DesignPatients with ACLF (n=41) were compared with healthy subjects (n=25) and patients with cirrhosis (n=22) or acute liver failure (n=30). CD14+CD15−CD11b+HLA-DR− cells were identified as per definition of M-MDSC and detailed immunophenotypic analyses were performed. Suppression of T cell activation was assessed by mixed lymphocyte reaction. Assessment of innate immune function included cytokine expression in response to Toll-like receptor (TLR-2, TLR-4 and TLR-9) stimulation and phagocytosis assays using flow cytometry and live cell imaging-based techniques.ResultsCirculating CD14+CD15−CD11b+HLA-DR− M-MDSCs were markedly expanded in patients with ACLF (55% of CD14+ cells). M-MDSC displayed immunosuppressive properties, significantly decreasing T cell proliferation (p=0.01), producing less tumour necrosis factor-alpha/interleukin-6 in response to TLR stimulation (all p<0.01), and reduced bacterial uptake of Escherichia coli (p<0.001). Persistently low expression of HLA-DR during disease evolution was linked to secondary infection and 28-day mortality. Recurrent TLR-2 and TLR-4 stimulation expanded M-MDSC in vitro. By contrast, TLR-3 agonism reconstituted HLA-DR expression and innate immune function ex vivo.ConclusionImmunosuppressive CD14+HLA-DR− M-MDSCs are expanded in patients with ACLF. They were depicted by suppressing T cell function, attenuated antimicrobial innate immune responses, linked to secondary infection, disease severity and prognosis. TLR-3 agonism reversed M-MDSC expansion and innate immune function and merits further evaluation as potential immunotherapeutic agent.</description><subject>Acute-On-Chronic Liver Failure - immunology</subject><subject>Adult</subject><subject>Anti-Infective Agents - therapeutic use</subject><subject>Cytokines - metabolism</subject><subject>Flow Cytometry</subject><subject>Fucosyltransferases - metabolism</subject><subject>Hepatology</subject><subject>HLA-DR Antigens - metabolism</subject><subject>Humans</subject><subject>Immune Tolerance - immunology</subject><subject>Immunology</subject><subject>Immunophenotyping</subject><subject>Lewis X Antigen - metabolism</subject><subject>Life Sciences</subject><subject>Lipopolysaccharide Receptors - metabolism</subject><subject>Lymphocyte Activation - immunology</subject><subject>Middle Aged</subject><subject>Myeloid-Derived Suppressor Cells - immunology</subject><subject>Phagocytosis - immunology</subject><subject>Polymerase Chain Reaction</subject><subject>Prognosis</subject><issn>0017-5749</issn><issn>1468-3288</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>9YT</sourceid><sourceid>ACMMV</sourceid><sourceid>EIF</sourceid><recordid>eNqNkc2KFDEUhYMozjj6Ai4kS0Wi-a_KRmh61BYaBNF1SCWp6TRVlTKp6mGeQNc-ok9iihoHdeUmCTnfPTe5B4CnBL8ihMnXV_N0HDpEMakQI5zU_B44J1zWiNG6vg_O8aKIiqsz8CjnI8a4rhV5CM5oLRTlrD4H37aXhL-EZRU_v_-Au_0GXX5aTv2N72JwyPkUTt7BPI9j8jnHBK3vugxDP5qQoBmm0AebYhNMBwsxxiH7Ig9wNFPww5ThdZgO0Nh58igOyB5SHIKFXfFNsDWhm5N_DB60psv-ye1-Ab68e_t5u0P7j-8_bDd71PCKT8hQLKi1qmKsMq510jbcOodNS5RqeKMsc8pKIaRrpROO4JYKKYVtjGiJcOwCvFl9x7npvbPlfcl0ekyhN-lGRxP038oQDvoqnrRQUjFJi8GL1eDwT9lus9fLHeZEsKpWJ1LY57fNUvw6-zzpPuRlembwcc6aKFwxKpjEBaUrWiaZc_LtnTfBeklbr2nrJW29pl2Knv35mbuS3_EWAK1A0x__x_AXV7259Q</recordid><startdate>20180601</startdate><enddate>20180601</enddate><creator>Bernsmeier, Christine</creator><creator>Triantafyllou, Evangelos</creator><creator>Brenig, Robert</creator><creator>Lebosse, Fanny J</creator><creator>Singanayagam, Arjuna</creator><creator>Patel, Vishal C</creator><creator>Pop, Oltin T</creator><creator>Khamri, Wafa</creator><creator>Nathwani, Rooshi</creator><creator>Tidswell, Robert</creator><creator>Weston, Christopher J</creator><creator>Adams, David H</creator><creator>Thursz, Mark R</creator><creator>Wendon, Julia A</creator><creator>Antoniades, Charalambos Gustav</creator><general>BMJ Publishing Group</general><general>Gut</general><scope>9YT</scope><scope>ACMMV</scope><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>7X8</scope><scope>1XC</scope><scope>VOOES</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-3411-1580</orcidid></search><sort><creationdate>20180601</creationdate><title>CD14+ CD15− HLA-DR− myeloid-derived suppressor cells impair antimicrobial responses in patients with acute-on-chronic liver failure</title><author>Bernsmeier, Christine ; Triantafyllou, Evangelos ; Brenig, Robert ; Lebosse, Fanny J ; Singanayagam, Arjuna ; Patel, Vishal C ; Pop, Oltin T ; Khamri, Wafa ; Nathwani, Rooshi ; Tidswell, Robert ; Weston, Christopher J ; Adams, David H ; Thursz, Mark R ; Wendon, Julia A ; Antoniades, Charalambos Gustav</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b474t-a2052cc97337adfd6cb4cdd0af199b4b9c3d9c6556df6d5d10f25665cba5f15d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Acute-On-Chronic Liver Failure - immunology</topic><topic>Adult</topic><topic>Anti-Infective Agents - therapeutic use</topic><topic>Cytokines - metabolism</topic><topic>Flow Cytometry</topic><topic>Fucosyltransferases - metabolism</topic><topic>Hepatology</topic><topic>HLA-DR Antigens - metabolism</topic><topic>Humans</topic><topic>Immune Tolerance - immunology</topic><topic>Immunology</topic><topic>Immunophenotyping</topic><topic>Lewis X Antigen - metabolism</topic><topic>Life Sciences</topic><topic>Lipopolysaccharide Receptors - metabolism</topic><topic>Lymphocyte Activation - immunology</topic><topic>Middle Aged</topic><topic>Myeloid-Derived Suppressor Cells - immunology</topic><topic>Phagocytosis - immunology</topic><topic>Polymerase Chain Reaction</topic><topic>Prognosis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bernsmeier, Christine</creatorcontrib><creatorcontrib>Triantafyllou, Evangelos</creatorcontrib><creatorcontrib>Brenig, Robert</creatorcontrib><creatorcontrib>Lebosse, Fanny J</creatorcontrib><creatorcontrib>Singanayagam, Arjuna</creatorcontrib><creatorcontrib>Patel, Vishal C</creatorcontrib><creatorcontrib>Pop, Oltin T</creatorcontrib><creatorcontrib>Khamri, Wafa</creatorcontrib><creatorcontrib>Nathwani, Rooshi</creatorcontrib><creatorcontrib>Tidswell, Robert</creatorcontrib><creatorcontrib>Weston, Christopher J</creatorcontrib><creatorcontrib>Adams, David H</creatorcontrib><creatorcontrib>Thursz, Mark R</creatorcontrib><creatorcontrib>Wendon, Julia A</creatorcontrib><creatorcontrib>Antoniades, Charalambos Gustav</creatorcontrib><collection>BMJ Open Access Journals</collection><collection>BMJ Journals:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><collection>Hyper Article en Ligne (HAL) (Open Access)</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Gut</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bernsmeier, Christine</au><au>Triantafyllou, Evangelos</au><au>Brenig, Robert</au><au>Lebosse, Fanny J</au><au>Singanayagam, Arjuna</au><au>Patel, Vishal C</au><au>Pop, Oltin T</au><au>Khamri, Wafa</au><au>Nathwani, Rooshi</au><au>Tidswell, Robert</au><au>Weston, Christopher J</au><au>Adams, David H</au><au>Thursz, Mark R</au><au>Wendon, Julia A</au><au>Antoniades, Charalambos Gustav</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CD14+ CD15− HLA-DR− myeloid-derived suppressor cells impair antimicrobial responses in patients with acute-on-chronic liver failure</atitle><jtitle>Gut</jtitle><addtitle>Gut</addtitle><date>2018-06-01</date><risdate>2018</risdate><volume>67</volume><issue>6</issue><spage>1155</spage><epage>1167</epage><pages>1155-1167</pages><issn>0017-5749</issn><eissn>1468-3288</eissn><abstract>ObjectiveImmune paresis in patients with acute-on-chronic liver failure (ACLF) accounts for infection susceptibility and increased mortality. Immunosuppressive mononuclear CD14+HLA-DR− myeloid-derived suppressor cells (M-MDSCs) have recently been identified to quell antimicrobial responses in immune-mediated diseases. We sought to delineate the function and derivation of M-MDSC in patients with ACLF, and explore potential targets to augment antimicrobial responses.DesignPatients with ACLF (n=41) were compared with healthy subjects (n=25) and patients with cirrhosis (n=22) or acute liver failure (n=30). CD14+CD15−CD11b+HLA-DR− cells were identified as per definition of M-MDSC and detailed immunophenotypic analyses were performed. Suppression of T cell activation was assessed by mixed lymphocyte reaction. Assessment of innate immune function included cytokine expression in response to Toll-like receptor (TLR-2, TLR-4 and TLR-9) stimulation and phagocytosis assays using flow cytometry and live cell imaging-based techniques.ResultsCirculating CD14+CD15−CD11b+HLA-DR− M-MDSCs were markedly expanded in patients with ACLF (55% of CD14+ cells). M-MDSC displayed immunosuppressive properties, significantly decreasing T cell proliferation (p=0.01), producing less tumour necrosis factor-alpha/interleukin-6 in response to TLR stimulation (all p<0.01), and reduced bacterial uptake of Escherichia coli (p<0.001). Persistently low expression of HLA-DR during disease evolution was linked to secondary infection and 28-day mortality. Recurrent TLR-2 and TLR-4 stimulation expanded M-MDSC in vitro. By contrast, TLR-3 agonism reconstituted HLA-DR expression and innate immune function ex vivo.ConclusionImmunosuppressive CD14+HLA-DR− M-MDSCs are expanded in patients with ACLF. They were depicted by suppressing T cell function, attenuated antimicrobial innate immune responses, linked to secondary infection, disease severity and prognosis. TLR-3 agonism reversed M-MDSC expansion and innate immune function and merits further evaluation as potential immunotherapeutic agent.</abstract><cop>England</cop><pub>BMJ Publishing Group</pub><pmid>28592438</pmid><doi>10.1136/gutjnl-2017-314184</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0002-3411-1580</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Gut, 2018-06, Vol.67 (6), p.1155-1167 |
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| subjects | Acute-On-Chronic Liver Failure - immunology Adult Anti-Infective Agents - therapeutic use Cytokines - metabolism Flow Cytometry Fucosyltransferases - metabolism Hepatology HLA-DR Antigens - metabolism Humans Immune Tolerance - immunology Immunology Immunophenotyping Lewis X Antigen - metabolism Life Sciences Lipopolysaccharide Receptors - metabolism Lymphocyte Activation - immunology Middle Aged Myeloid-Derived Suppressor Cells - immunology Phagocytosis - immunology Polymerase Chain Reaction Prognosis |
| title | CD14+ CD15− HLA-DR− myeloid-derived suppressor cells impair antimicrobial responses in patients with acute-on-chronic liver failure |
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