help button home button Am J Pathol PCR Enhanced. PCRboost from Biomatrica
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Hasegawa, S.
Right arrow Articles by Mitchell, R. N.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hasegawa, S.
Right arrow Articles by Mitchell, R. N.
(American Journal of Pathology. 1998;153:69-79.)
© 1998 American Society for Investigative Pathology

Regular Articles

Pattern of Graft- and Host-Specific MHC Class II Expression in Long-Term Murine Cardiac Allografts

Origin of Inflammatory and Vascular Wall Cells

Satoru Hasegawa* , Gerold Becker{dagger} , Hiroaki Nagano{ddagger} , Peter Libby* and Richard N. Mitchell{dagger}

From the Departments of Medicine,* Pathology,{dagger} and Surgery,{ddagger} Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts

In solid-tissue allografts, donor vascular cells as well as recipient inflammatory cells can express MHC class II molecules. However, it is uncertain how much residual donor endothelium persists and to what extent donor versus recipient MHC class II expression can contribute to the ongoing immune response, especially in long-term grafts. To establish the origin of class-II-expressing cells in the allograft, we evaluated the expression of donor- or recipient-specific MHC class II molecules in murine cardiac allografts. Donor hearts from BALB/c (H-2d) mice were transplanted into C57BL/6 (B6, H-2b) recipients; B6 isografts served as controls. Untreated allografts ceased functioning at approximately 7 days with severe parenchymal rejection. Allografts from recipients treated with anti-CD4 and anti-CD8 MAbs after transplantation were explanted at 8 to 12 weeks and demonstrated intimal fibroproliferative lesions with a mild parenchymal mononuclear cell infiltrate. Class II expression in isografts was limited to epicardial macrophages. Both acutely rejecting and long-term allografts contained abundant macrophages expressing recipient class II molecules. Occasional cells (passenger leukocytes) in untreated, acutely rejecting allografts bore donor class II molecules; long-term allografts contained few such cells. In contrast, vascular endothelial and medial smooth muscle cells consistently expressed donor class II molecules. These results suggest that ongoing MHC class II expression in donor vascular cells, as well as in recipient macrophages, may contribute to sustained activation of host T cells with consequent release of cytokines that ultimately promote the development of graft arteriosclerosis.




This article has been cited by other articles:


Home page
 J. Immunol.Home page
A. Valujskikh, Q. Zhang, and P. S. Heeger
CD8 T Cells Specific for a Donor-Derived, Self-Restricted Transplant Antigen Are Nonpathogenic Bystanders after Vascularized Heart Transplantation in Mice
J. Immunol., February 15, 2006; 176(4): 2190 - 2196.
[Abstract] [Full Text] [PDF]

Home page
 Cardiovasc ResHome page
Y. Furukawa, S. E Cole, R. V Shah, Y. Fukumoto, P. Libby, and R. N Mitchell
Wild-type but not interferon-{gamma}-deficient T cells induce graft arterial disease in the absence of B cells
Cardiovasc Res, August 1, 2004; 63(2): 347 - 356.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
T. J. Grazia, B. A. Pietra, Z. A. Johnson, B. P. Kelly, R. J. Plenter, and R. G. Gill
A Two-Step Model of Acute CD4 T-Cell Mediated Cardiac Allograft Rejection
J. Immunol., June 15, 2004; 172(12): 7451 - 7458.
[Abstract] [Full Text] [PDF]

Home page
 CirculationHome page
M. Ii and D. W. Losordo
Transplant Graft Vasculopathy: A Dark Side of Bone Marrow Stem Cells?
Circulation, December 23, 2003; 108(25): 3056 - 3058.
[Full Text] [PDF]

Home page
 CirculationHome page
P. Libby
Bone Marrow: A Fountain of Vascular Youth?
Circulation, July 29, 2003; 108(4): 378 - 379.
[Full Text] [PDF]

Home page
 Arterioscler. Thromb. Vasc. Bio.Home page
J.-L. Hillebrands, F. A. Klatter, and J. Rozing
Origin of Vascular Smooth Muscle Cells and the Role of Circulating Stem Cells in Transplant Arteriosclerosis
Arterioscler. Thromb. Vasc. Biol., March 1, 2003; 23(3): 380 - 387.
[Abstract] [Full Text] [PDF]

Home page
 Cardiovasc ResHome page
S. V. Subramanian, R. J. Kelm Jr., J. A. Polikandriotis, C. G. Orosz, and A. R. Strauch
Reprogramming of vascular smooth muscle {alpha}-actin gene expression as an early indicator of dysfunctional remodeling following heart transplant
Cardiovasc Res, June 1, 2002; 54(3): 539 - 548.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Pathol.Home page
J. Li, X. Han, J. Jiang, R. Zhong, G. M. Williams, J. G. Pickering, and L. H. Chow
Vascular Smooth Muscle Cells of Recipient Origin Mediate Intimal Expansion after Aortic Allotransplantation in Mice
Am. J. Pathol., June 1, 2001; 158(6): 1943 - 1947.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Pathol.Home page
Y. Furukawa, D. A. Mandelbrot, P. Libby, A. H. Sharpe, and R. N. Mitchell
Association of B7-1 Co-Stimulation with the Development of Graft Arterial Disease : Studies Using Mice Lacking B7-1, B7-2, or B7-1/B7-2
Am. J. Pathol., August 1, 2000; 157(2): 473 - 484.
[Abstract] [Full Text] [PDF]

Home page
 PERSPECT VASC SURG ENDOVASC THERHome page
J. Heckenkamp and G. M. Lamuraglia
Intimal Hyperplasia, Arterial Remodeling, and Restenosis: An Overview
Perspectives in Vascular Surgery and Endovascular Therapy, January 1, 1999; 11(2): 71 - 94.
[Abstract] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1998 by the American Society for Investigative Pathology.