Document Detail


Interleukin-17 antagonism inhibits acute but not chronic vascular rejection.
MedLine Citation:
PMID:  11477368     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Blocking the action of interleukin (IL) 17 with an IL-17 receptor (R):Fc fusion protein inhibits T-cell proliferative responses to alloantigens and prolongs vascularized heart graft survival. In this study, we examined whether IL-17 antagonism could suppress the development of chronic rejection. METHODS: A 0.6-cm section of C57BL10 (H2b) thoracic aorta was transplanted to recipient C3H (H2k) abdominal aorta. IL-17R:Fc or control human immunoglobulin G was administered i.p. (500 microg/day) from days 0 to 6 or from days 0 to 29. Mice were killed on days 7 or 30. Grafts were examined histologically and stained for alpha-smooth muscle actin (alpha-smA). Antidonor mixed leukocyte reaction, cytotoxic T cell, and alloantibody responses were quantified. RESULTS: On day 7, control grafts showed mononuclear cell (MNC) infiltration, pronounced endothelial damage, and apoptosis of intimal and medial cell compartments. By day 30, there was concentric intimal thickening, accumulation of alpha-smA+ cells, and collagen deposition. Patchy destruction of the elastic membranes and loss of alpha-smA expression in media were evident. IL-17R:Fc for 6 days decreased MNC infiltration in the intimal and medial compartments at day 7. The endothelium was preserved (completely or partially) in all grafts. The medial compartment showed normal alpha-smA expression. Irrespective of IL-17R:Fc treatment for either 6 days or continuously, allografts harvested at day 30 showed circumferential intimal thickening, with accumulation of alpha-smA+ cells and collagen deposition. There was no effect on circulating alloantibody levels. CONCLUSIONS: These findings support a role for IL-17 in the immunopathogenesis of acute vascular rejection and demonstrate the potential of IL-17 antagonism for therapy. By contrast, IL-17 antagonism does not appear to prevent ensuing chronic graft vascular disease, in particular neointimal formation.
Authors:
J L Tang; V M Subbotin; M A Antonysamy; A B Troutt; A S Rao; A W Thomson
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Transplantation     Volume:  72     ISSN:  0041-1337     ISO Abbreviation:  Transplantation     Publication Date:  2001 Jul 
Date Detail:
Created Date:  2001-07-30     Completed Date:  2001-08-23     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0132144     Medline TA:  Transplantation     Country:  United States    
Other Details:
Languages:  eng     Pagination:  348-50     Citation Subset:  IM    
Affiliation:
Thomas E. Starzl Transplantation Institute and Department of Surgery, University of Pittsburgh, W1544 Biomedical Science Tower, 200 Lothrop Street, Pittsburgh, PA 15213, USA. thomsonaw@msx.upmc.edu.
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MeSH Terms
Descriptor/Qualifier:
Acute Disease
Animals
Aorta, Abdominal / surgery
Aorta, Thoracic / surgery,  transplantation*
Chronic Disease
Complement System Proteins / immunology
Graft Rejection / prevention & control*
Humans
Immunoglobulin G / pharmacology
Interleukin-17 / antagonists & inhibitors,  immunology*
Isoantibodies / blood
Mice
Mice, Inbred C3H
Mice, Inbred C57BL
Receptors, Interleukin / therapeutic use*
Recombinant Fusion Proteins / therapeutic use
Transplantation, Homologous / immunology*
Grant Support
ID/Acronym/Agency:
DK 29961/DK/NIDDK NIH HHS; DK 49745/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Immunoglobulin G; 0/Interleukin-17; 0/Isoantibodies; 0/Receptors, Interleukin; 0/Recombinant Fusion Proteins; 0/rmIL-17R:huFc; 9007-36-7/Complement System Proteins

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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