| Bystander activation of iNKT cells occurs during conventional T-cell alloresponses. | |
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MedLine Citation:
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PMID: 22070799 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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It is well established that iNKT cells can be activated by both exogenous and a limited number of endogenous glycolipids. However, although iNKT cells have been implicated in the immune response to transplanted organs, the mechanisms by which iNKT cells are activated in this context remain unknown. Here we demonstrate that iNKT cells are not activated by allogeneic cells per se, but expand, both in vitro and in vivo, in the presence of a concomitant conventional T-cell response to alloantigen. This form of iNKT activation was found to occur independently of TCR-glycolipid/CD1d interactions but rather was a result of sequestration of IL-2 produced by conventional alloreactive T cells. These results show for the first time that IL-2, produced by activated conventional T cells, can activate iNKT cells independently of glycolipid/CD1d recognition. Therefore, we propose that the well-documented involvement of iNKT cells in autoimmunity, the control of cancer as well as following transplantation need not involve recognition of endogenous or exogenous glycolipids but alternatively may be a consequence of specific adaptive immune responses. |
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Authors:
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J-P Jukes; K J Wood; N D Jones |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2011-11-09 |
Journal Detail:
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Title: American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons Volume: 12 ISSN: 1600-6143 ISO Abbreviation: Am. J. Transplant. Publication Date: 2012 Mar |
Date Detail:
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Created Date: 2012-02-29 Completed Date: 2012-06-21 Revised Date: 2013-04-01 |
Medline Journal Info:
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Nlm Unique ID: 100968638 Medline TA: Am J Transplant Country: United States |
Other Details:
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Languages: eng Pagination: 590-9 Citation Subset: IM |
Copyright Information:
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© copyright 2011 The American Society of Transplantation and the American Society of Transplant Surgeons. |
Affiliation:
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Transplantation Research Immunology Group, Nuffield Department of Surgical Sciences, University of Oxford, John Radcliffe Hospital, Headington, Oxford, UK. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Antigen Presentation / immunology* Antigens, CD1d / immunology Apoptosis Blotting, Western Bystander Effect* Cell Proliferation Cells, Cultured Cytokines / genetics, metabolism Enzyme-Linked Immunosorbent Assay Female Flow Cytometry Graft Rejection / immunology Graft Survival / immunology Interleukin-2 / immunology*, metabolism Isoantigens / immunology Lymphocyte Activation / immunology* Male Mice Mice, Inbred BALB C Mice, Inbred C57BL Mice, Transgenic Natural Killer T-Cells / cytology, immunology*, metabolism* RNA, Messenger / genetics Real-Time Polymerase Chain Reaction Reverse Transcriptase Polymerase Chain Reaction Skin Transplantation / immunology* T-Lymphocytes / immunology* Transplantation Tolerance / immunology |
| Grant Support | |
ID/Acronym/Agency:
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082519//Wellcome Trust; //Medical Research Council; //Wellcome Trust |
| Chemical | |
Reg. No./Substance:
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0/Antigens, CD1d; 0/Cytokines; 0/Interleukin-2; 0/Isoantigens; 0/RNA, Messenger |
| Comments/Corrections | |
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