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Article: A negative regulatory role in mouse cardiac transplantation for a splice variant of CD80

TitleA negative regulatory role in mouse cardiac transplantation for a splice variant of CD80
Authors
Issue Date2006
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.transplantjournal.com
Citation
Transplantation, 2006, v. 82 n. 10, p. 1334-1341 How to Cite?
AbstractBACKGROUND. Members of the B7 costimulatory protein family (CD80 and CD86) play a determining role in allograft rejection. Both CD80 and CD86 have naturally occurring splice variants whose roles in transplantation are unknown. Full length CD80 has two immunoglobulin (Ig)-like domains in the extracellular portion, IgC and IgV. In mouse, the isoform IgV-CD80 lacks the IgC-like domain. Here we analyzed the role of mouse IgV-CD80 in heart allograft rejection and search for equivalent splice variants in human. METHODS. Mice made deficient for full-length CD80 but which retain expression of the shorter IgV-CD80 (CD80 mice) were used as donor or recipient of a heart allograft. Recipient animals were untreated or pretreated with alloantigen expressing cells and/or treated with CD80 and CTLA4 monoclonal antibodies (mAbs). RESULTS. Recipients expressing IgV-CD80 but not full length CD80 exhibited a slight prolongation in survival of either wild-type (Wt) or CD80 grafts. More dramatically, CD80 animals pretreated with donor alloantigen exhibited permanent graft survival, whereas their Wt counterparts rejected their grafts with a median survival of 24 days. This prolonged survival was due to the expression of IgV-CD80 in recipients since treatment with CD80 mAb abrogated the beneficial effect observed. We identified and report here a similar isoform of CD80 from human cDNA encoding a putative soluble, IgV-containing protein. CONCLUSIONS. IgV-CD80 bearing recipients show enhanced allograft survival especially after donor alloantigen pretreatment. This together with data from other species suggests that regulation delivered by splice variants of CD80 significantly modulates immunity and may be common across the species. © 2006 Lippincott Williams & Wilkins, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/172932
ISSN
2015 Impact Factor: 3.69
2015 SCImago Journal Rankings: 1.699
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorBugeon, Len_US
dc.contributor.authorWong, KKen_US
dc.contributor.authorRankin, AMen_US
dc.contributor.authorHargreaves, REGen_US
dc.contributor.authorDallman, MJen_US
dc.date.accessioned2012-10-30T06:25:52Z-
dc.date.available2012-10-30T06:25:52Z-
dc.date.issued2006en_US
dc.identifier.citationTransplantation, 2006, v. 82 n. 10, p. 1334-1341en_US
dc.identifier.issn0041-1337en_US
dc.identifier.urihttp://hdl.handle.net/10722/172932-
dc.description.abstractBACKGROUND. Members of the B7 costimulatory protein family (CD80 and CD86) play a determining role in allograft rejection. Both CD80 and CD86 have naturally occurring splice variants whose roles in transplantation are unknown. Full length CD80 has two immunoglobulin (Ig)-like domains in the extracellular portion, IgC and IgV. In mouse, the isoform IgV-CD80 lacks the IgC-like domain. Here we analyzed the role of mouse IgV-CD80 in heart allograft rejection and search for equivalent splice variants in human. METHODS. Mice made deficient for full-length CD80 but which retain expression of the shorter IgV-CD80 (CD80 mice) were used as donor or recipient of a heart allograft. Recipient animals were untreated or pretreated with alloantigen expressing cells and/or treated with CD80 and CTLA4 monoclonal antibodies (mAbs). RESULTS. Recipients expressing IgV-CD80 but not full length CD80 exhibited a slight prolongation in survival of either wild-type (Wt) or CD80 grafts. More dramatically, CD80 animals pretreated with donor alloantigen exhibited permanent graft survival, whereas their Wt counterparts rejected their grafts with a median survival of 24 days. This prolonged survival was due to the expression of IgV-CD80 in recipients since treatment with CD80 mAb abrogated the beneficial effect observed. We identified and report here a similar isoform of CD80 from human cDNA encoding a putative soluble, IgV-containing protein. CONCLUSIONS. IgV-CD80 bearing recipients show enhanced allograft survival especially after donor alloantigen pretreatment. This together with data from other species suggests that regulation delivered by splice variants of CD80 significantly modulates immunity and may be common across the species. © 2006 Lippincott Williams & Wilkins, Inc.en_US
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.transplantjournal.comen_US
dc.relation.ispartofTransplantationen_US
dc.subject.meshAlternative Splicing - Geneticsen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAntigens, Cd80 - Geneticsen_US
dc.subject.meshGenetic Variationen_US
dc.subject.meshGraft Survival - Immunologyen_US
dc.subject.meshHeart Transplantation - Immunologyen_US
dc.subject.meshHomeostasisen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Inbred C3hen_US
dc.subject.meshMice, Knockouten_US
dc.subject.meshModels, Animalen_US
dc.titleA negative regulatory role in mouse cardiac transplantation for a splice variant of CD80en_US
dc.typeArticleen_US
dc.identifier.emailWong, KK: kkywong@hkucc.hku.hken_US
dc.identifier.authorityWong, KK=rp01392en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1097/01.tp.0000239343.01775.54en_US
dc.identifier.pmid17130783-
dc.identifier.scopuseid_2-s2.0-33751517664en_US
dc.identifier.hkuros125294-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33751517664&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume82en_US
dc.identifier.issue10en_US
dc.identifier.spage1334en_US
dc.identifier.epage1341en_US
dc.identifier.isiWOS:000242461500012-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridBugeon, L=6602173647en_US
dc.identifier.scopusauthoridWong, KK=24438686400en_US
dc.identifier.scopusauthoridRankin, AM=7103152390en_US
dc.identifier.scopusauthoridHargreaves, REG=7007184704en_US
dc.identifier.scopusauthoridDallman, MJ=35473592200en_US

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