CD8+ T cells mediate aortic allograft vasculopathy by direct killing and an interferon-gamma-dependent indirect pathway.

[1]  P. Heeger,et al.  CD8 T Cells Can Reject Major Histocompatibility Complex Class I‐Deficient Skin Allografts , 2004, American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons.

[2]  R. Colvin,et al.  Further Analysis of the T‐Cell Subsets and Pathways of Murine Cardiac Allograft Rejection , 2003, American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons.

[3]  J. Légaré,et al.  Donor versus recipient: Neointimal cell origin in allograft vascular disease , 2002 .

[4]  A. Krasinskas,et al.  Depletion of recipient CD4+ but not CD8+ T lymphocytes prevents the development of cardiac allograft vasculopathy1 , 2002, Transplantation.

[5]  G. Hirsch,et al.  Recipient Cells Form the Intimal Proliferative Lesion in the Rat Aortic Model of Allograft Arteriosclerosis , 2002, American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons.

[6]  M. Yacoub,et al.  Indirect allorecognition can play an important role in the development of transplant arteriosclerosis. , 2002, Transplantation.

[7]  R. Colvin,et al.  Tolerance, Mixed Chimerism, and Chronic Transplant Arteriopathy1 2 , 2001, The Journal of Immunology.

[8]  J. Légaré,et al.  Prevention of allograft heart valve failure in a rat model. , 2001, The Journal of thoracic and cardiovascular surgery.

[9]  R. Novick,et al.  The Registry of the International Society for Heart and Lung Transplantation: eighteenth Official Report-2001. , 2001, The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation.

[10]  A. Stadnyk,et al.  Oral Exposure to Alloantigen Generates Intragraft CD8+ Regulatory Cells1 , 2001, The Journal of Immunology.

[11]  E. Popa,et al.  Origin of neointimal endothelium and alpha-actin-positive smooth muscle cells in transplant arteriosclerosis. , 2001, The Journal of clinical investigation.

[12]  P. Libby,et al.  Host bone-marrow cells are a source of donor intimal smooth- muscle–like cells in murine aortic transplant arteriopathy , 2001, Nature Medicine.

[13]  J. Schuman,et al.  Erratum: Ultrahigh-resolution ophthalmic optical coherence tomography (Nature Medicine (2000) 7 (502-507)) , 2001 .

[14]  R. Mitchell,et al.  CD8+ T cell subsets TC1 and TC2 cause different histopathologic forms of murine cardiac allograft rejection. , 2001, Transplantation.

[15]  J. Madsen,et al.  Indirect recognition of allopeptides promotes the development of cardiac allograft vasculopathy , 2001, Proceedings of the National Academy of Sciences of the United States of America.

[16]  A. Valujskikh,et al.  INDIRECTLY PRIMED CD8+ T CELLS ARE A PROMINENT COMPONENT OF THE ALLOGENEIC T-CELL REPERTOIRE AFTER SKIN GRAFT REJECTION IN MICE1 , 2001, Transplantation.

[17]  K. Wood,et al.  Development of a combined cardiac and aortic transplant model to investigate the development of transplant arteriosclerosis in the mouse. , 2000, The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation.

[18]  Y. Zhan,et al.  Prolonged allograft survival in anti-CD4 antibody transgenic mice: lack of residual helper T cells compared with other CD4-deficient mice. , 2000, Transplantation.

[19]  V. McAlister,et al.  Prolongation of allograft survival by Nippostrongylus brasiliensis is associated with decreased allospecific cytotoxic T lymphocyte activity and development of T cytotoxic cell type 2 cells. , 2000, Transplantation.

[20]  J. Pober,et al.  Interferon-γ elicits arteriosclerosis in the absence of leukocytes , 2000, Nature.

[21]  R. Liwski,et al.  Nematode infection enhances survival of activated T cells by modulating accessory cell function. , 1999, Journal of immunology.

[22]  T. Starzl,et al.  Marked mitigation of transplant vascular sclerosis in FasLgld (CD95L) mutant recipients. The role of alloantibodies in the development of chronic rejection. , 1999, Transplantation.

[23]  A. Djamali,et al.  Fas-mediated cytotoxicity is not required for rejection of murine nonvascularized heterotopic cardiac allografts. , 1998, Transplantation.

[24]  P. Libby,et al.  Interferon-gamma-secreting T-cell populations in rejecting murine cardiac allografts: assessment by flow cytometry. , 1998, The American journal of pathology.

[25]  J. Kearsey,et al.  Medial smooth muscle cell loss in arterial allografts occurs by cytolytic cell induced apoptosis. , 1998, European journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery.

[26]  Richard N. Mitchell,et al.  Coronary arteriosclerosis after T-cell-mediated injury in transplanted mouse hearts: role of interferon-gamma. , 1998, The American journal of pathology.

[27]  U. Heemann,et al.  Factors contributing to the development of chronic rejection in heterotopic rat heart transplantation. , 1997, Transplantation.

[28]  M. Mehra,et al.  Allograft aortopathy: an in vivo study of donor aorta involvement in cardiac allograft vasculopathy. , 1997, American heart journal.

[29]  T. Strom,et al.  Quantitative detection of immune activation transcripts as a diagnostic tool in kidney transplantation. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[30]  M. Billingham.  Pathology and etiology of chronic rejection of the heart. , 1994, Clinical transplantation.

[31]  J. Louis,et al.  Expansion of gamma interferon-producing CD8+ T cells following secondary infection of mice immune to Leishmania major , 1994, Infection and immunity.

[32]  H. Winn,et al.  Coronary atherosclerosis in transplanted mouse hearts. II. Importance of humoral immunity. , 1994, Journal of immunology.

[33]  R. Jaenisch,et al.  Mice lacking major histocompatibility complex class I and class II molecules. , 1993, Proceedings of the National Academy of Sciences of the United States of America.

[34]  M. Sitkovsky,et al.  Highly lytic CD8+, alpha beta T-cell receptor cytotoxic T cells with major histocompatibility complex (MHC) class I antigen-directed cytotoxicity in beta 2-microglobulin, MHC class I-deficient mice. , 1993, Proceedings of the National Academy of Sciences of the United States of America.

[35]  J. Fabre,et al.  Indirect T cell allorecognition: a cyclosporin A resistant pathway for T cell help for antibody production to donor MHC antigens. , 1993, Transplant immunology.

[36]  H. Ljunggren,et al.  Major histocompatibility complex class I-specific and -restricted killing of beta 2-microglobulin-deficient cells by CD8+ cytotoxic T lymphocytes. , 1992, Proceedings of the National Academy of Sciences of the United States of America.

[37]  W. Li,et al.  Cyclosporin A and FK506 mediate differential effects on T cell activation in vivo. , 1992, Journal of immunology.

[38]  P. Marrack,et al.  Normal development of mice deficient in beta 2M, MHC class I proteins, and CD8+ T cells. , 1990, Science.

[39]  R. Jaenisch,et al.  β2-Microglobulin deficient mice lack CD4−8+ cytolytic T cells , 1990, Nature.

[40]  B. Hall,et al.  Specific unresponsiveness in rats with prolonged cardiac allograft survival after treatment with cyclosporine. III. Further characterization of the CD4+ suppressor cell and its mechanisms of action , 1990, The Journal of experimental medicine.

[41]  J. Bellón,et al.  Function of inflammatory cells and neoral cyclosporin-A in heart transplant-associated coronary vasculopathy. , 2001, Histology and histopathology.

[42]  Y. Yoon,et al.  Cre/loxP-mediated excision and amplification of large segments of the Escherichia coli genome. , 1998, Genetic analysis : biomolecular engineering.

[43]  C. Giacomantonio,et al.  Development of a mouse aortic transplant model of chronic rejection , 1995, Microsurgery.