rdf:type |
|
lifeskim:mentions |
umls-concept:C0035015,
umls-concept:C0039194,
umls-concept:C0205178,
umls-concept:C0282554,
umls-concept:C0332448,
umls-concept:C0450127,
umls-concept:C0456387,
umls-concept:C0522536,
umls-concept:C0851827,
umls-concept:C1548437,
umls-concept:C1701901,
umls-concept:C1882923
|
pubmed:issue |
9
|
pubmed:dateCreated |
1999-11-19
|
pubmed:abstractText |
Direct evidence that cytokines with chemoattractant properties for leukocytes, chemokines, recruit alloantigen-primed T cells into transplanted allografts has been lacking. We present evidence that neutralization of a single chemokine inhibits T cell infiltration into class II MHC-disparate murine allografts and acute rejection. The chemokines IFN-gamma-inducible protein-10 and monokine induced by IFN-gamma (Mig) are expressed in allogeneic skin grafts during the late stages of acute rejection. Survival of class II MHC-disparate B6.H-2bm12 allografts is prolonged from day 14 to day 55 posttransplant when C57BL/6 recipients are given a short course treatment with an antiserum to Mig. This treatment also inhibits T cell and macrophage infiltration into the allografts. B6.H-2bm12 allografts are also not rejected by IFN-gamma-/- C57BL/6 recipients. Injection of Mig directly into B6.H-2bm12 grafts on IFN-gamma-deficient recipients restores T cell infiltration and rejection. Therefore, the inability of IFN-gamma-deficient recipients to reject the class II MHC-disparate allografts is due to the lack of intraallograft Mig production and alloantigen-primed T cell recruitment to the graft. These results indicate for the first time the potential utility of chemokine neutralization strategies in preventing T cell infiltration into allografts and abrogating acute rejection.
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pubmed:grant |
|
pubmed:language |
eng
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pubmed:journal |
|
pubmed:citationSubset |
AIM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CXCL10,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CXCL9,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokines, CXC,
http://linkedlifedata.com/resource/pubmed/chemical/Cxcl9 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Histocompatibility Antigens Class II,
http://linkedlifedata.com/resource/pubmed/chemical/Immune Sera,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger
|
pubmed:status |
MEDLINE
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pubmed:month |
Nov
|
pubmed:issn |
0022-1767
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pubmed:author |
|
pubmed:issnType |
Print
|
pubmed:day |
1
|
pubmed:volume |
163
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
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pubmed:pagination |
4878-85
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:10528189-Acute Disease,
pubmed-meshheading:10528189-Amino Acid Sequence,
pubmed-meshheading:10528189-Animals,
pubmed-meshheading:10528189-Cell Movement,
pubmed-meshheading:10528189-Chemokine CXCL10,
pubmed-meshheading:10528189-Chemokine CXCL9,
pubmed-meshheading:10528189-Chemokines, CXC,
pubmed-meshheading:10528189-Female,
pubmed-meshheading:10528189-Graft Rejection,
pubmed-meshheading:10528189-Graft Survival,
pubmed-meshheading:10528189-Histocompatibility Antigens Class II,
pubmed-meshheading:10528189-Immune Sera,
pubmed-meshheading:10528189-Injections, Intraperitoneal,
pubmed-meshheading:10528189-Interferon-gamma,
pubmed-meshheading:10528189-Mice,
pubmed-meshheading:10528189-Mice, Inbred A,
pubmed-meshheading:10528189-Mice, Inbred BALB C,
pubmed-meshheading:10528189-Mice, Inbred C57BL,
pubmed-meshheading:10528189-Mice, Knockout,
pubmed-meshheading:10528189-Molecular Sequence Data,
pubmed-meshheading:10528189-RNA, Messenger,
pubmed-meshheading:10528189-T-Lymphocytes,
pubmed-meshheading:10528189-Transplantation, Homologous
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pubmed:year |
1999
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pubmed:articleTitle |
T cell infiltration into class II MHC-disparate allografts and acute rejection is dependent on the IFN-gamma-induced chemokine Mig.
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pubmed:affiliation |
Department of Urology, Cleveland Clinic Foundation, OH 44195, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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