Paradoxical effects of interleukin-18 on the severity of acute graft-versus-host disease mediated by CD4+ and CD8+ T-cell subsets after experimental allogeneic bone marrow transplantation
Administration of exogenous interleukin-18 (IL-18) regulates experimental acute graft-versus-host disease (GVHD) in a Fas-dependent manner when donor CD4+ T cells are required for mortality after experimental allogeneic bone marrow transplantation (BMT). However, CD4+ and CD8+ T cells can induce acu...
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| Veröffentlicht in: | Blood 2004-11, Vol.104 (10), p.3393-3399 |
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| creator | Min, Chang-Ki Maeda, Yoshinobu Lowler, Kathleen Liu, Chen Clouthier, Shawn Lofthus, David Weisiger, Elizabeth Ferrara, James L.M. Reddy, Pavan |
| description | Administration of exogenous interleukin-18 (IL-18) regulates experimental acute graft-versus-host disease (GVHD) in a Fas-dependent manner when donor CD4+ T cells are required for mortality after experimental allogeneic bone marrow transplantation (BMT). However, CD4+ and CD8+ T cells can induce acute GVHD after clinical allogeneic BMT, and the role of IL-18 in CD8+-mediated acute GVHD is unknown. We, therefore, determined the role of IL-18 in GVHD mediated by CD4+ or CD8+ T cells across major histocompatibility complex (MHC) class II- and class I-disparate allogeneic BMT, respectively. Administering IL-18 significantly increased survival in CD4+-mediated GVHD but reduced survival in CD8+-mediated GVHD. This increase in deaths was associated with significantly greater clinical, biochemical, and histopathologic parameters of GVHD damage and was independent of Fas expression on donor T cells. Administering IL-18 significantly enhanced allospecific cytotoxic function and expansion of CD8+ cells. Endogenous IL-18 was critical to GVHD mediated by CD8+ donor T cells because IL-18 receptor-deficient donors caused significantly less GVHD but exacerbated CD4+-mediated, GVHD-related death. Furthermore, administering anti-IL-18 monoclonal antibody significantly reduced CD8+-mediated, GVHD-related death. Together these findings demonstrate that IL-18 has paradoxical effects on CD4+ and CD8+ cell-mediated GVHD. (Blood. 2004;104:3393-3399) |
| doi_str_mv | 10.1182/blood-2004-02-0763 |
| format | Article |
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However, CD4+ and CD8+ T cells can induce acute GVHD after clinical allogeneic BMT, and the role of IL-18 in CD8+-mediated acute GVHD is unknown. We, therefore, determined the role of IL-18 in GVHD mediated by CD4+ or CD8+ T cells across major histocompatibility complex (MHC) class II- and class I-disparate allogeneic BMT, respectively. Administering IL-18 significantly increased survival in CD4+-mediated GVHD but reduced survival in CD8+-mediated GVHD. This increase in deaths was associated with significantly greater clinical, biochemical, and histopathologic parameters of GVHD damage and was independent of Fas expression on donor T cells. Administering IL-18 significantly enhanced allospecific cytotoxic function and expansion of CD8+ cells. Endogenous IL-18 was critical to GVHD mediated by CD8+ donor T cells because IL-18 receptor-deficient donors caused significantly less GVHD but exacerbated CD4+-mediated, GVHD-related death. Furthermore, administering anti-IL-18 monoclonal antibody significantly reduced CD8+-mediated, GVHD-related death. Together these findings demonstrate that IL-18 has paradoxical effects on CD4+ and CD8+ cell-mediated GVHD. (Blood. 2004;104:3393-3399)</description><identifier>ISSN: 0006-4971</identifier><identifier>EISSN: 1528-0020</identifier><identifier>DOI: 10.1182/blood-2004-02-0763</identifier><identifier>PMID: 15280194</identifier><language>eng</language><publisher>Washington, DC: Elsevier Inc</publisher><subject>Acute Disease ; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy ; Animals ; Antibodies, Monoclonal - pharmacology ; Apoptosis - immunology ; Biological and medical sciences ; Bone Marrow Transplantation - immunology ; Bone marrow, stem cells transplantation. Graft versus host reaction ; CD4-Positive T-Lymphocytes - cytology ; CD4-Positive T-Lymphocytes - immunology ; CD8-Positive T-Lymphocytes - cytology ; CD8-Positive T-Lymphocytes - immunology ; Cytokines - metabolism ; Disease Models, Animal ; Female ; Graft vs Host Disease - drug therapy ; Graft vs Host Disease - immunology ; Graft vs Host Disease - mortality ; Histocompatibility Antigens Class I - immunology ; Histocompatibility Antigens Class II - immunology ; Interleukin-18 - antagonists & inhibitors ; Interleukin-18 - immunology ; Interleukin-18 - pharmacology ; Interleukin-18 Receptor alpha Subunit ; Medical sciences ; Mice ; Mice, Inbred C57BL ; Receptors, Interleukin - deficiency ; Receptors, Interleukin - genetics ; Receptors, Interleukin-18 ; Severity of Illness Index ; T-Lymphocytes, Cytotoxic - cytology ; T-Lymphocytes, Cytotoxic - immunology ; T-Lymphocytes, Cytotoxic - metabolism ; Transfusions. Complications. Transfusion reactions. Cell and gene therapy ; Transplantation, Homologous</subject><ispartof>Blood, 2004-11, Vol.104 (10), p.3393-3399</ispartof><rights>2004 American Society of Hematology</rights><rights>2005 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c426t-70c4f678bacd8e86332e087cee797a69cedfad75660dbb4214c6dcaec9b722033</citedby><cites>FETCH-LOGICAL-c426t-70c4f678bacd8e86332e087cee797a69cedfad75660dbb4214c6dcaec9b722033</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16347067$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15280194$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Min, Chang-Ki</creatorcontrib><creatorcontrib>Maeda, Yoshinobu</creatorcontrib><creatorcontrib>Lowler, Kathleen</creatorcontrib><creatorcontrib>Liu, Chen</creatorcontrib><creatorcontrib>Clouthier, Shawn</creatorcontrib><creatorcontrib>Lofthus, David</creatorcontrib><creatorcontrib>Weisiger, Elizabeth</creatorcontrib><creatorcontrib>Ferrara, James L.M.</creatorcontrib><creatorcontrib>Reddy, Pavan</creatorcontrib><title>Paradoxical effects of interleukin-18 on the severity of acute graft-versus-host disease mediated by CD4+ and CD8+ T-cell subsets after experimental allogeneic bone marrow transplantation</title><title>Blood</title><addtitle>Blood</addtitle><description>Administration of exogenous interleukin-18 (IL-18) regulates experimental acute graft-versus-host disease (GVHD) in a Fas-dependent manner when donor CD4+ T cells are required for mortality after experimental allogeneic bone marrow transplantation (BMT). However, CD4+ and CD8+ T cells can induce acute GVHD after clinical allogeneic BMT, and the role of IL-18 in CD8+-mediated acute GVHD is unknown. We, therefore, determined the role of IL-18 in GVHD mediated by CD4+ or CD8+ T cells across major histocompatibility complex (MHC) class II- and class I-disparate allogeneic BMT, respectively. Administering IL-18 significantly increased survival in CD4+-mediated GVHD but reduced survival in CD8+-mediated GVHD. This increase in deaths was associated with significantly greater clinical, biochemical, and histopathologic parameters of GVHD damage and was independent of Fas expression on donor T cells. Administering IL-18 significantly enhanced allospecific cytotoxic function and expansion of CD8+ cells. Endogenous IL-18 was critical to GVHD mediated by CD8+ donor T cells because IL-18 receptor-deficient donors caused significantly less GVHD but exacerbated CD4+-mediated, GVHD-related death. Furthermore, administering anti-IL-18 monoclonal antibody significantly reduced CD8+-mediated, GVHD-related death. Together these findings demonstrate that IL-18 has paradoxical effects on CD4+ and CD8+ cell-mediated GVHD. (Blood. 2004;104:3393-3399)</description><subject>Acute Disease</subject><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</subject><subject>Animals</subject><subject>Antibodies, Monoclonal - pharmacology</subject><subject>Apoptosis - immunology</subject><subject>Biological and medical sciences</subject><subject>Bone Marrow Transplantation - immunology</subject><subject>Bone marrow, stem cells transplantation. Graft versus host reaction</subject><subject>CD4-Positive T-Lymphocytes - cytology</subject><subject>CD4-Positive T-Lymphocytes - immunology</subject><subject>CD8-Positive T-Lymphocytes - cytology</subject><subject>CD8-Positive T-Lymphocytes - immunology</subject><subject>Cytokines - metabolism</subject><subject>Disease Models, Animal</subject><subject>Female</subject><subject>Graft vs Host Disease - drug therapy</subject><subject>Graft vs Host Disease - immunology</subject><subject>Graft vs Host Disease - mortality</subject><subject>Histocompatibility Antigens Class I - immunology</subject><subject>Histocompatibility Antigens Class II - immunology</subject><subject>Interleukin-18 - antagonists & inhibitors</subject><subject>Interleukin-18 - immunology</subject><subject>Interleukin-18 - pharmacology</subject><subject>Interleukin-18 Receptor alpha Subunit</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Receptors, Interleukin - deficiency</subject><subject>Receptors, Interleukin - genetics</subject><subject>Receptors, Interleukin-18</subject><subject>Severity of Illness Index</subject><subject>T-Lymphocytes, Cytotoxic - cytology</subject><subject>T-Lymphocytes, Cytotoxic - immunology</subject><subject>T-Lymphocytes, Cytotoxic - metabolism</subject><subject>Transfusions. Complications. Transfusion reactions. Cell and gene therapy</subject><subject>Transplantation, Homologous</subject><issn>0006-4971</issn><issn>1528-0020</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kc9u1DAQhyNERZfCC3BAvsClMowdr51IXNCWf1Klcihny7EnrSFrL7ZTus_Wl8NhV-qNky3rm59n5muaVwzeMdbx98MUo6McQFDgFJRsnzQrtuYdBeDwtFkBgKSiV-y0eZ7zTwAmWr5-1pwuELBerJqH7yYZF--9NRPBcURbMokj8aFgmnD-5QNlHYmBlFskGe8w-bJfCGPnguQmmbHQ-prnTG9jLsT5jCYj2aLzpqAjw55sLsQ5McHVS3dOrqnFaSJ5HjLW32oAJoL3uxq9xVBqI2aa4g0G9JYMMdQsk1L8Q0oyIe8mU5niY3jRnIxmyvjyeJ41Pz5_ut58pZdXX75tPl5SK7gsVIEVo1TdYKzrsJNtyxE6ZRFVr4zsLbrROLWWEtwwCM6Elc4atP2gOIe2PWveHnJ3Kf6eMRe99XkZwQSMc9ZSgWDrtq8gP4A2xZwTjnpXRzJprxnoRZn-p0wvyjRwvSirRa-P6fNQd_ZYcnRUgTdHwORqaaxLsD4_crIVCqSq3IcDh3UXdx6TztZjqOP5VLVqF_3_-vgLQo24UA</recordid><startdate>20041115</startdate><enddate>20041115</enddate><creator>Min, Chang-Ki</creator><creator>Maeda, Yoshinobu</creator><creator>Lowler, Kathleen</creator><creator>Liu, Chen</creator><creator>Clouthier, Shawn</creator><creator>Lofthus, David</creator><creator>Weisiger, Elizabeth</creator><creator>Ferrara, James L.M.</creator><creator>Reddy, Pavan</creator><general>Elsevier Inc</general><general>The Americain Society of Hematology</general><scope>6I.</scope><scope>AAFTH</scope><scope>IQODW</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></search><sort><creationdate>20041115</creationdate><title>Paradoxical effects of interleukin-18 on the severity of acute graft-versus-host disease mediated by CD4+ and CD8+ T-cell subsets after experimental allogeneic bone marrow transplantation</title><author>Min, Chang-Ki ; Maeda, Yoshinobu ; Lowler, Kathleen ; Liu, Chen ; Clouthier, Shawn ; Lofthus, David ; Weisiger, Elizabeth ; Ferrara, James L.M. ; Reddy, Pavan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c426t-70c4f678bacd8e86332e087cee797a69cedfad75660dbb4214c6dcaec9b722033</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Acute Disease</topic><topic>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</topic><topic>Animals</topic><topic>Antibodies, Monoclonal - pharmacology</topic><topic>Apoptosis - immunology</topic><topic>Biological and medical sciences</topic><topic>Bone Marrow Transplantation - immunology</topic><topic>Bone marrow, stem cells transplantation. Graft versus host reaction</topic><topic>CD4-Positive T-Lymphocytes - cytology</topic><topic>CD4-Positive T-Lymphocytes - immunology</topic><topic>CD8-Positive T-Lymphocytes - cytology</topic><topic>CD8-Positive T-Lymphocytes - immunology</topic><topic>Cytokines - metabolism</topic><topic>Disease Models, Animal</topic><topic>Female</topic><topic>Graft vs Host Disease - drug therapy</topic><topic>Graft vs Host Disease - immunology</topic><topic>Graft vs Host Disease - mortality</topic><topic>Histocompatibility Antigens Class I - immunology</topic><topic>Histocompatibility Antigens Class II - immunology</topic><topic>Interleukin-18 - antagonists & inhibitors</topic><topic>Interleukin-18 - immunology</topic><topic>Interleukin-18 - pharmacology</topic><topic>Interleukin-18 Receptor alpha Subunit</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Receptors, Interleukin - deficiency</topic><topic>Receptors, Interleukin - genetics</topic><topic>Receptors, Interleukin-18</topic><topic>Severity of Illness Index</topic><topic>T-Lymphocytes, Cytotoxic - cytology</topic><topic>T-Lymphocytes, Cytotoxic - immunology</topic><topic>T-Lymphocytes, Cytotoxic - metabolism</topic><topic>Transfusions. Complications. Transfusion reactions. Cell and gene therapy</topic><topic>Transplantation, Homologous</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Min, Chang-Ki</creatorcontrib><creatorcontrib>Maeda, Yoshinobu</creatorcontrib><creatorcontrib>Lowler, Kathleen</creatorcontrib><creatorcontrib>Liu, Chen</creatorcontrib><creatorcontrib>Clouthier, Shawn</creatorcontrib><creatorcontrib>Lofthus, David</creatorcontrib><creatorcontrib>Weisiger, Elizabeth</creatorcontrib><creatorcontrib>Ferrara, James L.M.</creatorcontrib><creatorcontrib>Reddy, Pavan</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Pascal-Francis</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><jtitle>Blood</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Min, Chang-Ki</au><au>Maeda, Yoshinobu</au><au>Lowler, Kathleen</au><au>Liu, Chen</au><au>Clouthier, Shawn</au><au>Lofthus, David</au><au>Weisiger, Elizabeth</au><au>Ferrara, James L.M.</au><au>Reddy, Pavan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Paradoxical effects of interleukin-18 on the severity of acute graft-versus-host disease mediated by CD4+ and CD8+ T-cell subsets after experimental allogeneic bone marrow transplantation</atitle><jtitle>Blood</jtitle><addtitle>Blood</addtitle><date>2004-11-15</date><risdate>2004</risdate><volume>104</volume><issue>10</issue><spage>3393</spage><epage>3399</epage><pages>3393-3399</pages><issn>0006-4971</issn><eissn>1528-0020</eissn><abstract>Administration of exogenous interleukin-18 (IL-18) regulates experimental acute graft-versus-host disease (GVHD) in a Fas-dependent manner when donor CD4+ T cells are required for mortality after experimental allogeneic bone marrow transplantation (BMT). However, CD4+ and CD8+ T cells can induce acute GVHD after clinical allogeneic BMT, and the role of IL-18 in CD8+-mediated acute GVHD is unknown. We, therefore, determined the role of IL-18 in GVHD mediated by CD4+ or CD8+ T cells across major histocompatibility complex (MHC) class II- and class I-disparate allogeneic BMT, respectively. Administering IL-18 significantly increased survival in CD4+-mediated GVHD but reduced survival in CD8+-mediated GVHD. This increase in deaths was associated with significantly greater clinical, biochemical, and histopathologic parameters of GVHD damage and was independent of Fas expression on donor T cells. Administering IL-18 significantly enhanced allospecific cytotoxic function and expansion of CD8+ cells. Endogenous IL-18 was critical to GVHD mediated by CD8+ donor T cells because IL-18 receptor-deficient donors caused significantly less GVHD but exacerbated CD4+-mediated, GVHD-related death. Furthermore, administering anti-IL-18 monoclonal antibody significantly reduced CD8+-mediated, GVHD-related death. Together these findings demonstrate that IL-18 has paradoxical effects on CD4+ and CD8+ cell-mediated GVHD. (Blood. 2004;104:3393-3399)</abstract><cop>Washington, DC</cop><pub>Elsevier Inc</pub><pmid>15280194</pmid><doi>10.1182/blood-2004-02-0763</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Acute Disease Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy Animals Antibodies, Monoclonal - pharmacology Apoptosis - immunology Biological and medical sciences Bone Marrow Transplantation - immunology Bone marrow, stem cells transplantation. Graft versus host reaction CD4-Positive T-Lymphocytes - cytology CD4-Positive T-Lymphocytes - immunology CD8-Positive T-Lymphocytes - cytology CD8-Positive T-Lymphocytes - immunology Cytokines - metabolism Disease Models, Animal Female Graft vs Host Disease - drug therapy Graft vs Host Disease - immunology Graft vs Host Disease - mortality Histocompatibility Antigens Class I - immunology Histocompatibility Antigens Class II - immunology Interleukin-18 - antagonists & inhibitors Interleukin-18 - immunology Interleukin-18 - pharmacology Interleukin-18 Receptor alpha Subunit Medical sciences Mice Mice, Inbred C57BL Receptors, Interleukin - deficiency Receptors, Interleukin - genetics Receptors, Interleukin-18 Severity of Illness Index T-Lymphocytes, Cytotoxic - cytology T-Lymphocytes, Cytotoxic - immunology T-Lymphocytes, Cytotoxic - metabolism Transfusions. Complications. Transfusion reactions. Cell and gene therapy Transplantation, Homologous |
| title | Paradoxical effects of interleukin-18 on the severity of acute graft-versus-host disease mediated by CD4+ and CD8+ T-cell subsets after experimental allogeneic bone marrow transplantation |
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