Publications
164 results found
Borozdenkova S, Smith J, Marshall S, et al., 2001, Identification of ICAM-1 polymorphism that is associated with protection from transplant associated vasculopathy after cardiac transplantation, HUMAN IMMUNOLOGY, Vol: 62, Pages: 247-255, ISSN: 0198-8859
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- Citations: 41
Raisky O, Morrison KJM, Obadia JF, et al., 2001, Acute rejection and cardiac graft vasculopathy in the absence of donor-derived ICAM-1 or P-selectin, JOURNAL OF HEART AND LUNG TRANSPLANTATION, Vol: 20, Pages: 340-349, ISSN: 1053-2498
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- Citations: 17
Newell H, Smith J, Pomerance A, et al., 2001, The effect of interleukin-6 gene polymorphisms on the outcome of cardiac transplantation., J Heart Lung Transplant, Vol: 20, Pages: 213-214
Rose ML, Danskine A, Smith JD, et al., 2000, Mycophenolate mofetil (MMF) depresses antibody production after cardiac transplantation, CIRCULATION, Vol: 102, Pages: 490-490, ISSN: 0009-7322
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- Citations: 2
Ensminger SM, Spriewald BM, Witzke O, et al., 2000, Intragraft interleukin-4 mRNA expression after short-term CD154 blockade may trigger delayed development of transplant arteriosclerosis in the absence of CD8+T cells, TRANSPLANTATION, Vol: 70, Pages: 955-963, ISSN: 0041-1337
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- Citations: 24
Lawson C, McCormack AM, Moyes D, et al., 2000, An epithelial cell line that can stimulate alloproliferation of resting CD4<SUP>+</SUP> T cells, but not after IFN-γ stimulation, JOURNAL OF IMMUNOLOGY, Vol: 165, Pages: 734-742, ISSN: 0022-1767
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- Citations: 11
Ensminger SM, Witzke O, Spriewald BM, et al., 2000, CD8<SUP>+</SUP> T cells contribute to the development of transplant arteriosclerosis despite CD154 blockade, TRANSPLANTATION, Vol: 69, Pages: 2609-2612, ISSN: 0041-1337
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- Citations: 68
Hornick PI, Mason PD, Baker RJ, et al., 2000, Significant frequencies of T cells with indirect anti-donor specificity in heart graft recipients with chronic rejection, CIRCULATION, Vol: 101, Pages: 2405-2410, ISSN: 0009-7322
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- Citations: 113
Ensminger SM, Witzke O, Spriewald BM, et al., 2000, Indirect allorecognition plays a pivotal role in the pathogenesis of transplant arteriosclerosis., TRANSPLANTATION, Vol: 69, Pages: S346-S346, ISSN: 0041-1337
Rose ML, 2000, Another way of presenting alloantigens to the immune system?, TRANSPLANTATION, Vol: 69, Pages: 1545-1546, ISSN: 0041-1337
Ensminger SM, Witzke O, Spriewald BM, et al., 2000, Eosinophils are major effector cells for the development of transplant arteriosclerosis and depend on the presence of IL-4., TRANSPLANTATION, Vol: 69, Pages: S299-S299, ISSN: 0041-1337
Smith JD, Lawson C, Yacoub MH, et al., 2000, Activation of NF-κB in human endothelial cells induced by monoclonal and allospecific HLA antibodies, INTERNATIONAL IMMUNOLOGY, Vol: 12, Pages: 563-571, ISSN: 0953-8178
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- Citations: 32
Yun S, Rose ML, Fabre JW, 2000, The induction of major histocompatibility complex class II expression is sufficient for the direct activation of human CD4+T cells by porcine vascular endothelial cells, TRANSPLANTATION, Vol: 69, Pages: 940-944, ISSN: 0041-1337
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- Citations: 18
Rose ML, 2000, Role of antibodies in transplant-associated cardiac allograft vasculopathy., Z Kardiol, Vol: 89 Suppl 9, Pages: IX/11-IX/15, ISSN: 0300-5860
Transplant-associated coronary artery disease or cardiac allograft vasculopathy is the major complication after cardiac transplantation. Here we discuss the role of antibodies and antibody-mediated activation of endothelial cells in the pathogenesis of this disease. Clinical and experimental studies have both described an association between chronic production of antibodies after transplantation and development of TxCAD. Although anti-HLA antibodies have been described in some cases, our studies suggest that antibodies against endothelial cells, for example, vimentin, are closely associated with disease development. It is known that indirect presentation of antigens, derived from the graft, probably drive chronic rejection. Here we are suggesting that minor antigens, released from damaged parenchymal cells within the graft, are responsible for the chronicity of the antibody response after transplantation. To date, only vimentin has been identified, but there may be a multiplicity of antigens. It is known that antibodies against endothelial cell surface molecules such as MHC class I and ICAM-1 can activate vascular cells (endothelial and smooth muscle cells) leading to exacerbation of the inflammatory response within the vessel wall. It remains to be seen whether antibodies against cytolytic proteins, released as a result of cell damage, cause cell activation; it may be that these antibodies are involved in clearance of apoptopic cells released from the graft.
Lidington EA, Moyes DL, McCormack AM, et al., 1999, A comparison of primary endothelial cells and endothelial cell lines for studies of immune interactions, TRANSPLANT IMMUNOLOGY, Vol: 7, Pages: 239-246, ISSN: 0966-3274
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- Citations: 129
Batten P, McCormack AM, Page CS, et al., 1999, Human T cell responses to human and procine endothelial cells are highly sensitive to cyclosporin A and FK506 in vitro, TRANSPLANTATION, Vol: 68, Pages: 1552-1560, ISSN: 0041-1337
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- Citations: 12
Rose ML, 1999, Allogeneic and xenogeneic interactions between endothelial cells and human T cells during transplant rejection, Conference on the Nato Advanced Study Institute on Vascular Endothelium - Mechanisms of Cell Signaling, Publisher: I O S PRESS, Pages: 33-47, ISSN: 0258-1213
Smith JD, Hornick PI, Rasmi N, et al., 1998, Effect of HLA mismatching and antibody status on "homovital" aortic valve homograft performance, ANNALS OF THORACIC SURGERY, Vol: 66, Pages: S212-S215, ISSN: 0003-4975
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- Citations: 42
Smith JD, Yacoub MH, Rose ML, 1998, Endothelial cell activation by sera containing HLA antibodies is mediated by interleukin-1, TRANSPLANTATION, Vol: 66, Pages: 1229-1237, ISSN: 0041-1337
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- Citations: 9
Rose ML, 1998, Endothelial cells as antigen-presenting cells: role in human transplant rejection, CELLULAR AND MOLECULAR LIFE SCIENCES, Vol: 54, Pages: 965-978, ISSN: 1420-682X
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- Citations: 67
Lidington EA, McCormack AM, Yacoub MH, et al., 1998, The effects of monocytes on the transendothelial migration of T lymphocytes, IMMUNOLOGY, Vol: 94, Pages: 221-227, ISSN: 0019-2805
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- Citations: 27
Jurcevic S, Dunn MJ, Crisp S, et al., 1998, A new enzyme-linked immunosorbent assay to measure anti-endothelial antibodies after cardiac transplantation demonstrates greater inhibition of antibody formation by tacrolimus compared with cyclosporine, TRANSPLANTATION, Vol: 65, Pages: 1197-1202, ISSN: 0041-1337
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- Citations: 34
Taylor-Robinson D, Ong G, Thomas BJ, et al., 1998, <i>Chlamydia pneumoniae</i> in vascular tissues from heart-transplant donors, LANCET, Vol: 351, Pages: 1255-1255, ISSN: 0140-6736
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- Citations: 25
Hornick PI, Mason PD, Yacoub MH, et al., 1998, Assessment of the contribution that direct allorecognition makes to the progression of chronic cardiac transplant rejection in humans, CIRCULATION, Vol: 97, Pages: 1257-1263, ISSN: 0009-7322
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- Citations: 103
McDouall RM, Batten P, McCormack A, et al., 1997, MHC class II expression on human heart microvascular endothelial cells - Exquisite sensitivity to interferon-gamma and natural killer cells, TRANSPLANTATION, Vol: 64, Pages: 1175-1180, ISSN: 0041-1337
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- Citations: 51
Hornick PI, Brookes PA, Mason PD, et al., 1997, Optimizing a limiting dilution culture system for quantifying the frequency of interleukin-2-producing alloreactive T helper lymphocytes, TRANSPLANTATION, Vol: 64, Pages: 472-479, ISSN: 0041-1337
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- Citations: 30
Johnson DL, Rose ML, Yacoub MH, 1997, Immunogenicity of human heart valve endothelial cells and fibroblasts, TRANSPLANTATION PROCEEDINGS, Vol: 29, Pages: 984-985, ISSN: 0041-1345
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- Citations: 14
Ferry BL, Welsh KI, Dunn MJ, et al., 1997, Anti-cell surface endothelial antibodies in sera from cardiac and kidney transplant recipients: Association with chronic rejection, TRANSPLANT IMMUNOLOGY, Vol: 5, Pages: 17-24, ISSN: 0966-3274
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- Citations: 58
Rose ML, 1997, Role of endothelial cells in allograft rejection., Vasc Med, Vol: 2, Pages: 105-114, ISSN: 1358-863X
The immunological properties of endothelial cells suggest they perform a pivotal role in acute and chronic rejection following solid organ transplantation. Their constitutive expression of MHC class II molecules (which initiate allograft rejection by activating CD4 T cells) and accessory molecules allows them to present foreign antigen by both the direct and indirect route to the recipient's immune system. The costimulatory molecules used by endothelial cells appear to differ from those used by traditional antigen-presenting cells such as B cells and dendritic cells. Release of non-HLA antigens from damaged endothelial cells results in a chronic antibody response--possibly contributing to graft vasculopathy and chronic rejection. Further understanding of the factors that regulate MHC class II and accessory molecule expression on endothelial cells could lead to novel strategies of therapeutic intervention.
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