IP-10-induced recruitment of CXCR3 + host T cells is required for small bowel allograft rejection
Background & Aims : Chemokines mediate cell trafficking in inflammatory states such as allograft rejection. However, their role in small-bowel allograft rejection has not been defined. The aim of this study was to examine the roles of type 1 helper T-cell chemokines in small-bowel allograft reje...
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| Veröffentlicht in: | Gastroenterology (New York, N.Y. 1943) N.Y. 1943), 2004-03, Vol.126 (3), p.809-818 |
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| container_title | Gastroenterology (New York, N.Y. 1943) |
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| creator | Zhang, Zheng Kaptanoglu, Levent Tang, Yueming Ivancic, David Rao, Sambasiva M. Luster, Andrew Barrett, Terrence A. Fryer, Jonathan |
| description | Background & Aims
:
Chemokines mediate cell trafficking in inflammatory states such as allograft rejection. However, their role in small-bowel allograft rejection has not been defined. The aim of this study was to examine the roles of type 1 helper T-cell chemokines in small-bowel allograft rejection.
Methods
:
Mucosal histology, chemokine messenger RNA (real-time polymerase chain reaction), and cell isolates were examined in small-bowel allografts and isografts. Interferon-γ-inducible protein-10/ CXC chemokine receptor (CXCR) 3 interactions were specifically evaluated by using allografts from interferon-γ-inducible protein-10
−/− donors and adoptive transfer of CXCR3
−/− T cells into recombination activating gene (RAG)-1
−/− recipients of small-bowel allografts.
Results
:
Type 1 helper T-cell cytokine (interferon-γ) and chemokine (interferon-γ-inducible protein-10, monokine induced by interferon-γ, macrophage-inflammatory protein-1α, and regulated on activation, normal T cells expressed and secreted) messenger RNA up-regulation was detected (real-time polymerase chain reaction) by postoperative day 3 in small-bowel allografts. Interferon-γ-inducible protein-10
+/+ small-bowel allograft rejection was associated with a dramatic (>7-fold) increase in CXCR3
+ host T cells in the graft lamina propria. With interferon-γ-inducible protein-10
−/− small-bowel allografts, CXCR3
+ host T-cell infiltration of the graft lamina propria was markedly decreased and rejection was significantly delayed. Whereas adoptive transfer of wild-type B6 (CXCR3
+/+) T cells into B6 (RAG-1
−/−) recipients induced rapid rejection of CB6F1 small-bowel allografts, rejection was significantly delayed (29.2 ± 8.7 days vs. 16.5 ± 3.1 days;
P < 0.01) in B6 (RAG-1
−/−) mice reconstituted with T cells from B6 (CXCR3
−/−) mice.
Conclusions
:
Recruitment of CXCR3
+ host T cells by donor derived interferon-γ-inducible protein-10 may precipitate small-bowel allograft rejection. These data highlight the importance of type 1 helper T cell-related chemokines in promoting cell-mediated rejection responses in small-bowel allografts and suggest that interferon-γ-inducible protein-10 is an attractive therapeutic target for humanized monoclonal antibody strategies. |
| doi_str_mv | 10.1053/j.gastro.2003.12.014 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_71682765</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0016508503020559</els_id><sourcerecordid>71682765</sourcerecordid><originalsourceid>FETCH-LOGICAL-c358t-acd966945042a1d5f853230b89939553ab237437472839b2c59d824e40651d7d3</originalsourceid><addsrcrecordid>eNp9kMtKxDAUQIMoOj7-QCQrN9KaR9MmG0EGXyAoMoK7kCbpmKFtNEkV_94MM-BOuHDv4tzXAeAUoxIjRi9X5VLFFHxJEKIlJiXC1Q6YYUZ4gRAmu2CWU10wxNkBOIxxhRASlON9cIArwTmnbAbUw3OBUeFGM2lrYLA6TC4NdkzQd3D-Nn-h8AK--5jgAmrb9xG6mLHPyYXMdz7AOKi-h63_tj3MlV8G1aWMrKxOzo_HYK9TfbQn23wEXm9vFvP74vHp7mF-_VhoyngqlDairkXFUEUUNqzjjBKKWi4EFYxR1RLaVDkawqloiWbCcFLZCtUMm8bQI3C-mfsR_OdkY5KDi-uL1Wj9FGWDa06ammWw2oA6-BiD7eRHcIMKPxIjuVYrV3KjVq7VSkxkVpvbzrbzp3aw5q9p6zIDVxvA5i-_nA0yamfHrDWr0kka7_7f8AvURYnY</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>71682765</pqid></control><display><type>article</type><title>IP-10-induced recruitment of CXCR3 + host T cells is required for small bowel allograft rejection</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals</source><source>Alma/SFX Local Collection</source><creator>Zhang, Zheng ; Kaptanoglu, Levent ; Tang, Yueming ; Ivancic, David ; Rao, Sambasiva M. ; Luster, Andrew ; Barrett, Terrence A. ; Fryer, Jonathan</creator><creatorcontrib>Zhang, Zheng ; Kaptanoglu, Levent ; Tang, Yueming ; Ivancic, David ; Rao, Sambasiva M. ; Luster, Andrew ; Barrett, Terrence A. ; Fryer, Jonathan</creatorcontrib><description>Background & Aims
:
Chemokines mediate cell trafficking in inflammatory states such as allograft rejection. However, their role in small-bowel allograft rejection has not been defined. The aim of this study was to examine the roles of type 1 helper T-cell chemokines in small-bowel allograft rejection.
Methods
:
Mucosal histology, chemokine messenger RNA (real-time polymerase chain reaction), and cell isolates were examined in small-bowel allografts and isografts. Interferon-γ-inducible protein-10/ CXC chemokine receptor (CXCR) 3 interactions were specifically evaluated by using allografts from interferon-γ-inducible protein-10
−/− donors and adoptive transfer of CXCR3
−/− T cells into recombination activating gene (RAG)-1
−/− recipients of small-bowel allografts.
Results
:
Type 1 helper T-cell cytokine (interferon-γ) and chemokine (interferon-γ-inducible protein-10, monokine induced by interferon-γ, macrophage-inflammatory protein-1α, and regulated on activation, normal T cells expressed and secreted) messenger RNA up-regulation was detected (real-time polymerase chain reaction) by postoperative day 3 in small-bowel allografts. Interferon-γ-inducible protein-10
+/+ small-bowel allograft rejection was associated with a dramatic (>7-fold) increase in CXCR3
+ host T cells in the graft lamina propria. With interferon-γ-inducible protein-10
−/− small-bowel allografts, CXCR3
+ host T-cell infiltration of the graft lamina propria was markedly decreased and rejection was significantly delayed. Whereas adoptive transfer of wild-type B6 (CXCR3
+/+) T cells into B6 (RAG-1
−/−) recipients induced rapid rejection of CB6F1 small-bowel allografts, rejection was significantly delayed (29.2 ± 8.7 days vs. 16.5 ± 3.1 days;
P < 0.01) in B6 (RAG-1
−/−) mice reconstituted with T cells from B6 (CXCR3
−/−) mice.
Conclusions
:
Recruitment of CXCR3
+ host T cells by donor derived interferon-γ-inducible protein-10 may precipitate small-bowel allograft rejection. These data highlight the importance of type 1 helper T cell-related chemokines in promoting cell-mediated rejection responses in small-bowel allografts and suggest that interferon-γ-inducible protein-10 is an attractive therapeutic target for humanized monoclonal antibody strategies.</description><identifier>ISSN: 0016-5085</identifier><identifier>EISSN: 1528-0012</identifier><identifier>DOI: 10.1053/j.gastro.2003.12.014</identifier><identifier>PMID: 14988835</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Chemokine CXCL10 ; Chemokines - genetics ; Chemokines, CXC - deficiency ; Chemokines, CXC - metabolism ; Cytokines - genetics ; Graft Rejection - etiology ; Graft Rejection - pathology ; Graft Rejection - physiopathology ; Intestine, Small - pathology ; Intestine, Small - transplantation ; Male ; Mice ; Mice, Inbred Strains ; Mice, Knockout ; Phenotype ; Postoperative Period ; Receptors, CCR5 - metabolism ; Receptors, Chemokine - metabolism ; Receptors, CXCR3 ; RNA, Messenger - metabolism ; T-Lymphocytes - metabolism ; T-Lymphocytes - pathology ; Tissue Donors ; Transplantation, Homologous</subject><ispartof>Gastroenterology (New York, N.Y. 1943), 2004-03, Vol.126 (3), p.809-818</ispartof><rights>2004 American Gastroenterological Association</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c358t-acd966945042a1d5f853230b89939553ab237437472839b2c59d824e40651d7d3</citedby><cites>FETCH-LOGICAL-c358t-acd966945042a1d5f853230b89939553ab237437472839b2c59d824e40651d7d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1053/j.gastro.2003.12.014$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3536,27903,27904,45974</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14988835$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Zheng</creatorcontrib><creatorcontrib>Kaptanoglu, Levent</creatorcontrib><creatorcontrib>Tang, Yueming</creatorcontrib><creatorcontrib>Ivancic, David</creatorcontrib><creatorcontrib>Rao, Sambasiva M.</creatorcontrib><creatorcontrib>Luster, Andrew</creatorcontrib><creatorcontrib>Barrett, Terrence A.</creatorcontrib><creatorcontrib>Fryer, Jonathan</creatorcontrib><title>IP-10-induced recruitment of CXCR3 + host T cells is required for small bowel allograft rejection</title><title>Gastroenterology (New York, N.Y. 1943)</title><addtitle>Gastroenterology</addtitle><description>Background & Aims
:
Chemokines mediate cell trafficking in inflammatory states such as allograft rejection. However, their role in small-bowel allograft rejection has not been defined. The aim of this study was to examine the roles of type 1 helper T-cell chemokines in small-bowel allograft rejection.
Methods
:
Mucosal histology, chemokine messenger RNA (real-time polymerase chain reaction), and cell isolates were examined in small-bowel allografts and isografts. Interferon-γ-inducible protein-10/ CXC chemokine receptor (CXCR) 3 interactions were specifically evaluated by using allografts from interferon-γ-inducible protein-10
−/− donors and adoptive transfer of CXCR3
−/− T cells into recombination activating gene (RAG)-1
−/− recipients of small-bowel allografts.
Results
:
Type 1 helper T-cell cytokine (interferon-γ) and chemokine (interferon-γ-inducible protein-10, monokine induced by interferon-γ, macrophage-inflammatory protein-1α, and regulated on activation, normal T cells expressed and secreted) messenger RNA up-regulation was detected (real-time polymerase chain reaction) by postoperative day 3 in small-bowel allografts. Interferon-γ-inducible protein-10
+/+ small-bowel allograft rejection was associated with a dramatic (>7-fold) increase in CXCR3
+ host T cells in the graft lamina propria. With interferon-γ-inducible protein-10
−/− small-bowel allografts, CXCR3
+ host T-cell infiltration of the graft lamina propria was markedly decreased and rejection was significantly delayed. Whereas adoptive transfer of wild-type B6 (CXCR3
+/+) T cells into B6 (RAG-1
−/−) recipients induced rapid rejection of CB6F1 small-bowel allografts, rejection was significantly delayed (29.2 ± 8.7 days vs. 16.5 ± 3.1 days;
P < 0.01) in B6 (RAG-1
−/−) mice reconstituted with T cells from B6 (CXCR3
−/−) mice.
Conclusions
:
Recruitment of CXCR3
+ host T cells by donor derived interferon-γ-inducible protein-10 may precipitate small-bowel allograft rejection. These data highlight the importance of type 1 helper T cell-related chemokines in promoting cell-mediated rejection responses in small-bowel allografts and suggest that interferon-γ-inducible protein-10 is an attractive therapeutic target for humanized monoclonal antibody strategies.</description><subject>Animals</subject><subject>Chemokine CXCL10</subject><subject>Chemokines - genetics</subject><subject>Chemokines, CXC - deficiency</subject><subject>Chemokines, CXC - metabolism</subject><subject>Cytokines - genetics</subject><subject>Graft Rejection - etiology</subject><subject>Graft Rejection - pathology</subject><subject>Graft Rejection - physiopathology</subject><subject>Intestine, Small - pathology</subject><subject>Intestine, Small - transplantation</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred Strains</subject><subject>Mice, Knockout</subject><subject>Phenotype</subject><subject>Postoperative Period</subject><subject>Receptors, CCR5 - metabolism</subject><subject>Receptors, Chemokine - metabolism</subject><subject>Receptors, CXCR3</subject><subject>RNA, Messenger - metabolism</subject><subject>T-Lymphocytes - metabolism</subject><subject>T-Lymphocytes - pathology</subject><subject>Tissue Donors</subject><subject>Transplantation, Homologous</subject><issn>0016-5085</issn><issn>1528-0012</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kMtKxDAUQIMoOj7-QCQrN9KaR9MmG0EGXyAoMoK7kCbpmKFtNEkV_94MM-BOuHDv4tzXAeAUoxIjRi9X5VLFFHxJEKIlJiXC1Q6YYUZ4gRAmu2CWU10wxNkBOIxxhRASlON9cIArwTmnbAbUw3OBUeFGM2lrYLA6TC4NdkzQd3D-Nn-h8AK--5jgAmrb9xG6mLHPyYXMdz7AOKi-h63_tj3MlV8G1aWMrKxOzo_HYK9TfbQn23wEXm9vFvP74vHp7mF-_VhoyngqlDairkXFUEUUNqzjjBKKWi4EFYxR1RLaVDkawqloiWbCcFLZCtUMm8bQI3C-mfsR_OdkY5KDi-uL1Wj9FGWDa06ammWw2oA6-BiD7eRHcIMKPxIjuVYrV3KjVq7VSkxkVpvbzrbzp3aw5q9p6zIDVxvA5i-_nA0yamfHrDWr0kka7_7f8AvURYnY</recordid><startdate>20040301</startdate><enddate>20040301</enddate><creator>Zhang, Zheng</creator><creator>Kaptanoglu, Levent</creator><creator>Tang, Yueming</creator><creator>Ivancic, David</creator><creator>Rao, Sambasiva M.</creator><creator>Luster, Andrew</creator><creator>Barrett, Terrence A.</creator><creator>Fryer, Jonathan</creator><general>Elsevier Inc</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>7X8</scope></search><sort><creationdate>20040301</creationdate><title>IP-10-induced recruitment of CXCR3 + host T cells is required for small bowel allograft rejection</title><author>Zhang, Zheng ; Kaptanoglu, Levent ; Tang, Yueming ; Ivancic, David ; Rao, Sambasiva M. ; Luster, Andrew ; Barrett, Terrence A. ; Fryer, Jonathan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c358t-acd966945042a1d5f853230b89939553ab237437472839b2c59d824e40651d7d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Animals</topic><topic>Chemokine CXCL10</topic><topic>Chemokines - genetics</topic><topic>Chemokines, CXC - deficiency</topic><topic>Chemokines, CXC - metabolism</topic><topic>Cytokines - genetics</topic><topic>Graft Rejection - etiology</topic><topic>Graft Rejection - pathology</topic><topic>Graft Rejection - physiopathology</topic><topic>Intestine, Small - pathology</topic><topic>Intestine, Small - transplantation</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred Strains</topic><topic>Mice, Knockout</topic><topic>Phenotype</topic><topic>Postoperative Period</topic><topic>Receptors, CCR5 - metabolism</topic><topic>Receptors, Chemokine - metabolism</topic><topic>Receptors, CXCR3</topic><topic>RNA, Messenger - metabolism</topic><topic>T-Lymphocytes - metabolism</topic><topic>T-Lymphocytes - pathology</topic><topic>Tissue Donors</topic><topic>Transplantation, Homologous</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Zheng</creatorcontrib><creatorcontrib>Kaptanoglu, Levent</creatorcontrib><creatorcontrib>Tang, Yueming</creatorcontrib><creatorcontrib>Ivancic, David</creatorcontrib><creatorcontrib>Rao, Sambasiva M.</creatorcontrib><creatorcontrib>Luster, Andrew</creatorcontrib><creatorcontrib>Barrett, Terrence A.</creatorcontrib><creatorcontrib>Fryer, Jonathan</creatorcontrib><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>Gastroenterology (New York, N.Y. 1943)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Zheng</au><au>Kaptanoglu, Levent</au><au>Tang, Yueming</au><au>Ivancic, David</au><au>Rao, Sambasiva M.</au><au>Luster, Andrew</au><au>Barrett, Terrence A.</au><au>Fryer, Jonathan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>IP-10-induced recruitment of CXCR3 + host T cells is required for small bowel allograft rejection</atitle><jtitle>Gastroenterology (New York, N.Y. 1943)</jtitle><addtitle>Gastroenterology</addtitle><date>2004-03-01</date><risdate>2004</risdate><volume>126</volume><issue>3</issue><spage>809</spage><epage>818</epage><pages>809-818</pages><issn>0016-5085</issn><eissn>1528-0012</eissn><abstract>Background & Aims
:
Chemokines mediate cell trafficking in inflammatory states such as allograft rejection. However, their role in small-bowel allograft rejection has not been defined. The aim of this study was to examine the roles of type 1 helper T-cell chemokines in small-bowel allograft rejection.
Methods
:
Mucosal histology, chemokine messenger RNA (real-time polymerase chain reaction), and cell isolates were examined in small-bowel allografts and isografts. Interferon-γ-inducible protein-10/ CXC chemokine receptor (CXCR) 3 interactions were specifically evaluated by using allografts from interferon-γ-inducible protein-10
−/− donors and adoptive transfer of CXCR3
−/− T cells into recombination activating gene (RAG)-1
−/− recipients of small-bowel allografts.
Results
:
Type 1 helper T-cell cytokine (interferon-γ) and chemokine (interferon-γ-inducible protein-10, monokine induced by interferon-γ, macrophage-inflammatory protein-1α, and regulated on activation, normal T cells expressed and secreted) messenger RNA up-regulation was detected (real-time polymerase chain reaction) by postoperative day 3 in small-bowel allografts. Interferon-γ-inducible protein-10
+/+ small-bowel allograft rejection was associated with a dramatic (>7-fold) increase in CXCR3
+ host T cells in the graft lamina propria. With interferon-γ-inducible protein-10
−/− small-bowel allografts, CXCR3
+ host T-cell infiltration of the graft lamina propria was markedly decreased and rejection was significantly delayed. Whereas adoptive transfer of wild-type B6 (CXCR3
+/+) T cells into B6 (RAG-1
−/−) recipients induced rapid rejection of CB6F1 small-bowel allografts, rejection was significantly delayed (29.2 ± 8.7 days vs. 16.5 ± 3.1 days;
P < 0.01) in B6 (RAG-1
−/−) mice reconstituted with T cells from B6 (CXCR3
−/−) mice.
Conclusions
:
Recruitment of CXCR3
+ host T cells by donor derived interferon-γ-inducible protein-10 may precipitate small-bowel allograft rejection. These data highlight the importance of type 1 helper T cell-related chemokines in promoting cell-mediated rejection responses in small-bowel allografts and suggest that interferon-γ-inducible protein-10 is an attractive therapeutic target for humanized monoclonal antibody strategies.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>14988835</pmid><doi>10.1053/j.gastro.2003.12.014</doi><tpages>10</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0016-5085 |
| ispartof | Gastroenterology (New York, N.Y. 1943), 2004-03, Vol.126 (3), p.809-818 |
| issn | 0016-5085 1528-0012 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_71682765 |
| source | MEDLINE; Elsevier ScienceDirect Journals; Alma/SFX Local Collection |
| subjects | Animals Chemokine CXCL10 Chemokines - genetics Chemokines, CXC - deficiency Chemokines, CXC - metabolism Cytokines - genetics Graft Rejection - etiology Graft Rejection - pathology Graft Rejection - physiopathology Intestine, Small - pathology Intestine, Small - transplantation Male Mice Mice, Inbred Strains Mice, Knockout Phenotype Postoperative Period Receptors, CCR5 - metabolism Receptors, Chemokine - metabolism Receptors, CXCR3 RNA, Messenger - metabolism T-Lymphocytes - metabolism T-Lymphocytes - pathology Tissue Donors Transplantation, Homologous |
| title | IP-10-induced recruitment of CXCR3 + host T cells is required for small bowel allograft rejection |
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