Ischemic preconditioning in the liver is independent of regulatory T cell activity
Ischemic preconditioning (IPC) protects organs from ischemia reperfusion injury (IRI) through unknown mechanisms. Effector T cell populations have been implicated in the pathogenesis of IRI, and T regulatory cells (Treg) have become a putative therapeutic target, with suggested involvement in IPC. W...
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Published in | PloS one Vol. 7; no. 11; p. e49647 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
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Public Library of Science
21.11.2012
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Abstract | Ischemic preconditioning (IPC) protects organs from ischemia reperfusion injury (IRI) through unknown mechanisms. Effector T cell populations have been implicated in the pathogenesis of IRI, and T regulatory cells (Treg) have become a putative therapeutic target, with suggested involvement in IPC. We explored the role of Treg in hepatic IRI and IPC in detail. IPC significantly reduced injury following ischemia reperfusion insults. Treg were mobilized rapidly to the circulation and liver after IRI, but IPC did not further increase Treg numbers, nor was it associated with modulation of circulating pro-inflammatory chemokine or cytokine profiles. We used two techniques to deplete Treg from mice prior to IRI. Neither Treg depleted FoxP3.LuciDTR mice, nor wildtyoe mice depleted of Tregs with PC61, were more susceptible to IRI compared with controls. Despite successful enrichment of Treg in the liver, by adoptive transfer of both iTreg and nTreg or by in vivo expansion of Treg with IL-2/anti-IL-2 complexes, no protection against IRI was observed.We have explored the role of Treg in IRI and IPC using a variety of techniques to deplete and enrich them within both the liver and systemically. This work represents an important negative finding that Treg are not implicated in IPC and are unlikely to have translational potential in hepatic IRI. |
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AbstractList | Ischemic preconditioning (IPC) protects organs from ischemia reperfusion injury (IRI) through unknown mechanisms. Effector T cell populations have been implicated in the pathogenesis of IRI, and T regulatory cells (Treg) have become a putative therapeutic target, with suggested involvement in IPC. We explored the role of Treg in hepatic IRI and IPC in detail. IPC significantly reduced injury following ischemia reperfusion insults. Treg were mobilized rapidly to the circulation and liver after IRI, but IPC did not further increase Treg numbers, nor was it associated with modulation of circulating pro-inflammatory chemokine or cytokine profiles. We used two techniques to deplete Treg from mice prior to IRI. Neither Treg depleted FoxP3.LuciDTR mice, nor wildtyoe mice depleted of Tregs with PC61, were more susceptible to IRI compared with controls. Despite successful enrichment of Treg in the liver, by adoptive transfer of both iTreg and nTreg or by in vivo expansion of Treg with IL-2/anti-IL-2 complexes, no protection against IRI was observed.We have explored the role of Treg in IRI and IPC using a variety of techniques to deplete and enrich them within both the liver and systemically. This work represents an important negative finding that Treg are not implicated in IPC and are unlikely to have translational potential in hepatic IRI. |
Audience | Academic |
Author | Borthwick, Gary Howie, A Forbes Richards, James A Clay, Spike Howie, Sarah E M Wigmore, Stephen J Anderton, Stephen M Devey, Luke R O'Connor, Richard A |
AuthorAffiliation | Centre for Inflammation Research, The Queen’s Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom CNRS, France |
AuthorAffiliation_xml | – name: Centre for Inflammation Research, The Queen’s Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom – name: CNRS, France |
Author_xml | – sequence: 1 givenname: Luke R surname: Devey fullname: Devey, Luke R email: luke@devey.net organization: Centre for Inflammation Research, The Queen's Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom. luke@devey.net – sequence: 2 givenname: James A surname: Richards fullname: Richards, James A – sequence: 3 givenname: Richard A surname: O'Connor fullname: O'Connor, Richard A – sequence: 4 givenname: Gary surname: Borthwick fullname: Borthwick, Gary – sequence: 5 givenname: Spike surname: Clay fullname: Clay, Spike – sequence: 6 givenname: A Forbes surname: Howie fullname: Howie, A Forbes – sequence: 7 givenname: Stephen J surname: Wigmore fullname: Wigmore, Stephen J – sequence: 8 givenname: Stephen M surname: Anderton fullname: Anderton, Stephen M – sequence: 9 givenname: Sarah E M surname: Howie fullname: Howie, Sarah E M |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/23185394$$D View this record in MEDLINE/PubMed |
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CitedBy_id | crossref_primary_10_1111_tri_12723 crossref_primary_10_3390_jcm6070069 crossref_primary_10_1371_journal_pone_0106892 crossref_primary_10_1016_j_trim_2017_08_002 crossref_primary_10_1371_journal_pone_0138688 crossref_primary_10_1681_ASN_2013050502 crossref_primary_10_1016_j_ajpath_2015_07_007 |
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Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Conceived and designed the experiments: LRD JAR RO’C SJW SMA SEMH. Performed the experiments: LRD JAR GB SC AFH. Analyzed the data: LRD. Contributed reagents/materials/analysis tools: R O’C SMA. Wrote the paper: LRD JAR RO’C AFH SJW SMA SEMH. Competing Interests: The authors have declared that no competing interests exist. |
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Snippet | Ischemic preconditioning (IPC) protects organs from ischemia reperfusion injury (IRI) through unknown mechanisms. Effector T cell populations have been... |
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SubjectTerms | Adenosine Adoptive transfer Animals Antigens Chemokines - metabolism Cytokines Cytokines - metabolism Depletion Experiments Flow Cytometry - methods Foxp3 protein Green Fluorescent Proteins - metabolism Health aspects Immunology Immunoregulation Inflammation Injury prevention Interleukin 2 Interleukin-2 - metabolism Ischemia Ischemic Preconditioning - methods Liver Liver - metabolism Liver - pathology Lymphocytes Lymphocytes T Medical research Medicine Mice Mice, Inbred C57BL Organs Pathogenesis Physiology Preconditioning Reperfusion Reperfusion Injury Rodents Spleen - cytology T cells T-Lymphocytes, Regulatory - cytology Transcription factors Transplants & implants |
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Title | Ischemic preconditioning in the liver is independent of regulatory T cell activity |
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