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Journal articles on the topic 'Chronic vascular rejection'

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Published: 29 March 2025

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1

KEMNITZ, J. "Chronic rejection?Graft vascular disease." Human Pathology 26, no. 4 (April 1995): 462. http://dx.doi.org/10.1016/0046-8177(95)90151-5.

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2

Zheng, S.-X., R. D. C. Forbes, M. Gomersall, and R. D. Guttmann. "Retransplantation and reversibility of chronic vascular rejection." Transplantation Proceedings 29, no. 1-2 (February 1997): 1541. http://dx.doi.org/10.1016/s0041-1345(96)00667-7.

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3

Karnovsky, Morris J., Mary E. Russell, Wayne Hancock, Mohamed H. Sayegh, and David H. Adams. "Chronic rejection in experimental cardiac transplantation in a rat model." Clinical Transplantation 8, no. 3pt2 (June 1994): 308–12. http://dx.doi.org/10.1111/j.1399-0012.1994.tb00259.x.

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The most significant pathologic finding in chronically rejected organ grafts is diffuse concentric intimal proliferation in the arterial system. To develop a reproducible model of chronic vascular rejection in cardiac grafts which we could then use to study the pathogenesis and therapy of this disease process, we exchanged heterotopic cardiac allografts across minor histocompatibility barriers using commercially available Lewis rats as donors and F‐344 rats as recipients. We found that all long‐term surviving allografts developed diffuse graft arteriosclerotic lesions which were virtually identical in appearance to those seen in chronically rejected human cardiac grafts. Immunohistochemical studies confirm that end‐stage lesions arc similar in composition to human lesions and are made up predominantly of vascular smooth muscle cells with occasional monocytes and T cells. Analysis of continuous series of rejecting allografts demonstrates that a distinct inflammatory stage precedes smooth muscle cell accumulation in areas of intimal thickening, suggesting that mononuclear cells play a role in the developing lesion. Endothelial expression of class II and ICAM‐1 probably underlies early mononuclear cell adherence to the endothelium. Analysis using quantitative RT‐PCR and immunocytochemistry confirms MCP‐I is expressed by ED I‐positive monocyte/macrophages in rejecting cardiac grafts, suggesting this chemoattractant may help drive mononuclear cell accumulation in the expanding intima. Immunohistochemical labelling of PDGF, TNF and IL‐1β in vascular lesions suggests these factors may trigger intimal vascular smooth muscle cell proliferation in chronically rejecting allografts, as they, along with protein S, were closely associated with sites of intimal hyperplasia and smooth muscle cell proliferation. Hypercholesterolemia did not enhance the severity of lesion development in long‐term surviving allografts, suggesting that lipid levels are not a major etiologic factor in graft arteriosclerotic lesion formation in the Lewis‐F‐344 model. Placing the recipients on a diet deficient in essential fatty acids (which modulates leukocyte functions and infiltration) reduced graft infiltration by mononuclear cells and markedly diminished arterial lesion development in chronically rejecting grafts. A key role for CD4 and mononuclear cells (T cells and/or macrophages) in the initiation and amplification of the vascular response is suggested because a short course of CD4 mAb‐ targeted therapy attenuated many of the vascular sequelae of chronic allograft rejection; there was an absence of myocardial necrosis, a lack of upregulation of ICAM and class II MHC antigens, and decreased expression of TNF, IL‐Iβ, TGF‐β, PDGF and protein S expression. Our data suggest that the activated macrophage is a major force in driving the system toward accelerated atherosclerosis, and that this model should prove useful in analyzing the pathogenesis and drug therapy of chronic rejection.
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4

Sijpkens, Y. W. J., J. A. Bruijn, and L. C. Paul. "Chronic allograft nephropathy categorised in chronic interstitial and vascular rejection." Transplantation Proceedings 33, no. 1-2 (February 2001): 1153. http://dx.doi.org/10.1016/s0041-1345(00)02438-6.

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5

Rustom, Rana, J. Steve Grime, R. A. Sells, A. Amara, M. J. Jackson, Alan Shenkin, Paul Maltby, et al. "RENAL TUBULAR PEPTIDE CATABOLISM IN CHRONIC VASCULAR REJECTION." Renal Failure 23, no. 3-4 (January 2001): 517–31. http://dx.doi.org/10.1081/jdi-100104734.

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6

Sibley, Richard K. "Morphologic features of chronic rejection in kidney and less commonly transplanted organs." Clinical Transplantation 8, no. 3pt2 (June 1994): 293–98. http://dx.doi.org/10.1111/j.1399-0012.1994.tb00256.x.

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Chronic rejection is characterized by morphological evidence of destruction of the transplanted organ. The injury to the organ is associated with collagenization of variable degree. The destruction and fibrosis of the organ is probably the result of 1) direct alloimmune cytotoxic injury (i.e., acute and/or ongoing rejection) of the organ tissue, and 2) end‐organ ischemic injury secondary to fibroproliferative endarteritis (i.e.. chronic vascular rejection). The cardinal morphological feature of chronic rejection in all allografts is fibroproliferative endarteritis, which is characterized by widening of the subendothelial space due to a cellular fibrosis which may have an onion‐skin appearance with a PAS or silver stain. Macrophages with foamy cytoplasm and lymphocytes may be present in this fibrotic tissue. The smooth muscle wall may show foci of fibrosis as well, if involved by previous necrotizing rejection. These features are commonly found in needle core biopsies of kidney allografts and may involve the interlobular, arcuate, and interlobar arteries. They are less commonly found in pancreatic needle biopsies, and only rarely in hepatic and pulmonary allograft biopsies, rendering the diagnosis of chronic rejection often difficult to establish. Though the vascular lesions may not be apparent in biopsies, they are typically found in explained organs where larger vessels can be examined. Thus, the diagnosis of chronic rejection may rest upon other and in some instances less specific abnormalities, usually ischemic in origin due to vascular lesions and consequent decreased perfusion of the graft. In the kidney these changes are characterized by strips of cortical atrophy (tubular atrophy, interstitial fibrosis and collapsed glomerular tufts) and infarcts, in the liver by centrolobular ballooning degeneration and canalicular cholestasis, and in the pancreas by chronic pancreatitis and infarcts. In lung allografts, the major and only reliable morphological feature of chronic rejection is bronchiolitis obliterans. Additional features of chronic rejection include onion‐skinning of glomerular capillary walls (chronic transplant glomerulopathy) in the kidney, chronic active hepatitis and paucity of bile ducts in the liver, and destruction of the islets in pancreas allografts.
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7

Billingham, Margaret E. "Pathology and etiology of chronic rejection of the heart." Clinical Transplantation 8, no. 3pt2 (June 1994): 289–92. http://dx.doi.org/10.1111/j.1399-0012.1994.tb00255.x.

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As there are other lesions in the cardiac allografts of long‐term survivors, it is best to refer to the vascular lesion as “graft vascular disease”. Graft vascular disease may be evident as early as 3 months after cardiac transplantation and may cause death in the recipient as late as 22 years post‐transplant. The disease affects infants, children, and adults as well as the recipients of combined heart‐lung transplants. It is one of the most discouraging aspects of long‐term survival in combined heart‐lung and heart transplantation, accounting for 18% of the deaths among the 201 cardiac transplants performed at Stanford during the cyclosporine era. The pathology of graft vascular disease is that of a concentric intimai proliferation with minimal damage to the elastic lamina and minimal or no change in the media of the coronary vessel wall. The lesion may affect the entire length of the vessel wall as well as the branches and small branches that penetrate into the myocardium of the coronary system. These changes differ from that of naturally occurring atherosclerosis in that, instead of focal lesions developing, the whole length of the vessel is affected, including the small branches. This precludes optimal treatment with angioplasty and other therapies. Because small vessels are involved, the resulting myocardial infarcts may be patchy and small. Presently, no strong correlation has been made with usual risk factors or transplantation for end‐stage coronary atherosclerosis, cardiomyopathy or congenital heart disease. The etiology of graft coronary disease remains unclear. Studies have suggested vascular cell activation of various kinds, including cytokines. Some of these processes, however, have been found in nontransplant coronary disease as well. A correlation with acute rejection, although suspected, has not been definitively proved; in combined heart‐ lung transplantation, the cardiac graft rarely rejects and yet graft vascular disease develops. The only correlation thus far has been with cytomegalovirus (CVM) infection, in which death from graft vascular disease is higher in infected recipients. More recently, a correlation has been made with the so‐called “Quilty lesion”. Early animal studies with in vivo blockade of tumor necrosis factor (TNF) indicated that it inhibits the development of graft arteriopathy. Such studies are being conducted extensively in America and elsewhere.
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8

Dimény, Emöke, Bengt Fellström, Erik Larsson, Gunnar Tufveson, and Hans Lithell. "Chronic vascular rejection and hyperlipoproteinemia in renal transplant patients." Clinical Transplantation 7, no. 5 (October 1993): 482–90. http://dx.doi.org/10.1111/j.1399-0012.1993.tb00726.x.

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The lipoprotein pattern was investigated in 46 renal transplant recipients with histologically confirmed chronic vascular rejection (CVR) as an approach to studying its role for development and progression of CVR or transplant atherosclerosis. Renal transplant patients without evidence of chronic rejection and other renal patients with varying degrees of renal function impairment and/or proteinuria served as controls. Patients with CVR had more advanced lipoprotein disturbances as compared to patients with stable graft function. CVR patients had higher VLDL, LDL and total cholesterol and triglyceride levels, a more triglyceride‐rich VLDL and LDL fraction and a more atherogenic distribution of the lipoproteins as compared to control renal transplant patients. Impaired renal function and proteinuria, which are common in CVR, explain these lipid abnormalities only in part, since patients with CVR constitute a different cluster in this respect when compared with other patients with renal dysfunction. It is concluded that lipoprotein abnormalities and oxidative modification may play a crucial role for a growth factor‐driven progression of CVR.
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9

SWAN, SUZANNE K., GRETCHEN S. CRARY, CARLOS GUIJARRO, MICHAEL P. OʼDONNELL, WILLIAM F. KEANE, and BERTRAM L. KASISKE. "IMMUNOSUPPRESSIVE EFFECTS OF LEFLUNOMIDE IN EXPERIMENTAL CHRONIC VASCULAR REJECTION." Transplantation 60, no. 8 (October 1995): 887–90. http://dx.doi.org/10.1097/00007890-199510000-00025.

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10

SWAN, SUZANNE K., GRETCHEN S. CRARY, CARLOS GUIJARRO, MICHAEL P. OʼDONNELL, WILLIAM F. KEANE, and BERTRAM L. KASISKE. "IMMUNOSUPPRESSIVE EFFECTS OF LEFLUNOMIDE IN EXPERIMENTAL CHRONIC VASCULAR REJECTION." Transplantation 60, no. 8 (October 1995): 887–90. http://dx.doi.org/10.1097/00007890-199510270-00025.

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11

Shimizu, Tomokazu, Kazuya Omoto, Hideki Ishida, and Kazunari Tanabe. "Clinicopathologic Analyses of Chronic Vascular Rejection After Kidney Transplantation." Transplantation Proceedings 52, no. 6 (July 2020): 1769–74. http://dx.doi.org/10.1016/j.transproceed.2020.02.128.

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12

Häyry, Pekka, Ari Mennander, Anne Räisänen-Sokolowski, Jarkko Ustinov, Karl Lemström, Päivi Aho, Serdar Yilmaz, Irmeli Lautenschlager, and Timo Paavonen. "Pathophysiology of vascular wall changes in chronic allograft rejection." Transplantation Reviews 7, no. 1 (January 1993): 1–20. http://dx.doi.org/10.1016/s0955-470x(05)80007-2.

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13

VAN SAASE, JAN L. C. M., FOKKO J. VAN DER WOUDE, JANE THOROGOOD, ADRIANUS A. M. J. HOLLANDER, LEENDERT A. VAN ES, JAN J. WEENING, J. HAJO VAN BOCKEL, and JAN ANTHONIE BRUIJN. "THE RELATION BETWEEN ACUTE VASCULAR AND INTERSTITIAL RENAL ALLOGRAFT REJECTION AND SUBSEQUENT CHRONIC REJECTION." Transplantation 59, no. 9 (May 1995): 1280–84. http://dx.doi.org/10.1097/00007890-199505000-00010.

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14

VAN SAASE, JAN L. C. M., FOKKO J. VAN DER WOUDE, JANE THOROGOOD, ADRIANUS A. M. J. HOLLANDER, LEENDERT A. VAN ES, JAN J. WEENING, J. HAJO VAN BOCKEL, and JAN ANTHONIE BRUIJN. "THE RELATION BETWEEN ACUTE VASCULAR AND INTERSTITIAL RENAL ALLOGRAFT REJECTION AND SUBSEQUENT CHRONIC REJECTION." Transplantation 59, no. 9 (May 1995): 1280–84. http://dx.doi.org/10.1097/00007890-199505150-00010.

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15

Häyry, P., E. Aavik, M. Sarwal, D. Du Toit, and J. Vamvakopoulos. "CHRONIC REJECTION: PROSPECTS FOR THERAPEUTIC INTERVENTION IN FIBROPROLIFERATIVE VASCULAR DISEASE." Tissue Antigens 60, no. 6 (December 2002): 560. http://dx.doi.org/10.1034/j.1399-0039.2002.00036.x.

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16

Yacoub-Youssef, H., B. Marcheix, D. Calise, J. C. Thiers, H. Benoist, N. Blaes, B. Ségui, C. Dambrin, and M. Thomsen. "Chronic Vascular Rejection: Histologic Comparison Between Two Murine Experimental Models." Transplantation Proceedings 37, no. 6 (July 2005): 2886–87. http://dx.doi.org/10.1016/j.transproceed.2005.05.030.

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17

Richter, M., H. R. Richter, H. G. Olbrich, and F. W. Mohr. "Do vascular compartments differ in the development of chronic rejection?" Journal of Heart and Lung Transplantation 20, no. 2 (February 2001): 186. http://dx.doi.org/10.1016/s1053-2498(00)00384-3.

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18

Wieczorek, G., M. Bigaud, K. Menninger, S. Riesen, V. Quesniaux, H. J. Schuurman, M. Audet, A. Blancher, M. J. Mihatsch, and V. Nickeleit. "Acute and Chronic Vascular Rejection in Nonhuman Primate Kidney Transplantation." American Journal of Transplantation 6, no. 6 (June 2006): 1285–96. http://dx.doi.org/10.1111/j.1600-6143.2006.01307.x.

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19

Azuma, Haruhito, Uwe W. Heemann, Stefan G. Tullius, and Nicholas L. Tilney. "Cytokines and adhesion molecules in chronic rejection." Clinical Transplantation 8, no. 2pt2 (April 1994): 168–80. http://dx.doi.org/10.1111/j.1399-0012.1994.tb00092.x.

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Despite the increasing short‐term success of clinical transplantation during recent years, many allografts, regardless of organ type, continue to be lost over the long term due to chronic rejection, despite improvements in immunosuppression and better patient management. Thus, as a long‐term answer to an irreversible disease process, organ transplantation has not lived up to its potential. Although the host mechanisms leading to the process remain obscure, the progressive morphological changes evolving in the afflicted organs are well understood. Chronic rejection has long been thought to be an antibody‐mediated event, as immunoglobulins and other circulating proteins are often associated with areas of vascular damage. It is becoming more clear, however, that a whole array of host defense factors, primarily, cytokines, lymphokines and adhesion molecules, are of critical importance in the process. This review summarizes various cytokines and their individual functions as well as adhesion molecules potentially involved in aspects of immune responsiveness, and placed in the context of chronic rejection.
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20

Paul, Leendert C. "Functional and histologic characteristics of chronic renal allograft rejection." Clinical Transplantation 8, no. 3pt2 (June 1994): 319–23. http://dx.doi.org/10.1111/j.1399-0012.1994.tb00261.x.

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Chronic allograft rejection very probably results from the inter‐actions between allogeneic immune injury, tissue reactions in response to injury, and local intragraft hemodynamic adaptations to the progressive loss of functioning organ mass. We examined each of these components in a rat model of chronic renal allograft rejection. Although immunofluorescence studies of renal allografts with chronic rejection usually reveal nondiagnostic patterns of immunoglobulin deposits, we found, using Western blot analysis, donor‐directed antibodies against novel glomerular basement membrane antigens in the sera of animals with chronic rejection‐associated transplant glomerulopathy. Stop‐flow micropuncture studies have shown that the glomerular capillary pressure in transplanted kidneys resembles that of the donor strain kidney in response to renal ablation. Northern blots for growth factor transcripts showed induced expression of mRNA levels for various growth factors in long‐surviving renal transplants. Reduction in intraglomerular pressure was associated with increased recipient survival, preservation of renal function, decreased amounts of proteinuria, and less severe structural lesions in the glomeruli. We conclude that the glomerular lesions of chronic rejection may arise from a combination of antiglomerular (allo) antibodies in conjunction with increased intraglomerular pressures and local production of growth factors. The vascular lesions and interstitial scarring of chronic rejection. may arise from previous episodes of graft vasculitis and interstitial inflammation, respectively.
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21

Geraghty, James G., Richard L. Stoltenberg, Hans W. Sollinger, and Deb A. Hullett. "VASCULAR SMOOTH MUSCLE CELLS AND NEOINTIMAL HYPERPLASIA IN CHRONIC TRANSPLANT REJECTION." Transplantation 62, no. 4 (August 1996): 502–9. http://dx.doi.org/10.1097/00007890-199608270-00013.

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22

Ball, B., C. Mousson, C. Ratignier, F. Guignier, D. Glotz, and G. Rifle. "Antibodies to vascular endothelial cells in chronic rejection of renal allografts." Transplantation Proceedings 32, no. 2 (March 2000): 353–54. http://dx.doi.org/10.1016/s0041-1345(99)00976-8.

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23

Nolan, Charles R., Kristin P. Saenz, Charles A. Thomas, and Kim D. Murphy. "Role of the eosinophil in chronic vascular rejection of renal allografts." American Journal of Kidney Diseases 26, no. 4 (October 1995): 634–42. http://dx.doi.org/10.1016/0272-6386(95)90601-0.

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24

Shimizu, Tomokazu, Hiroshi Toma, Rumi Shibahara, Kuniko Tsunoyama, Junpei Izuka, Taiji Nozaki, Hideki Ishida, Kazunari Tanabe, Kazuho Honda, and Junki Koike. "Clinical and pathological analyses of chronic vascular rejection after kidney transplantation." Nephrology 20 (June 2, 2015): 20–25. http://dx.doi.org/10.1111/nep.12464.

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25

Hasnain, Mujtaba Ali, Samrah Mujtaba, Iqra Javed, Misbah ., Muhammad Shahzad Gul, and Abdul Ghaffar. "Determine the Effect of Immunosuppressant on follicular regulatory T-cells in kidney transplant patients." Pakistan Journal of Medical and Health Sciences 15, no. 10 (October 30, 2021): 2689–91. http://dx.doi.org/10.53350/pjmhs2115102689.

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Background: Over the last few years, there are two major problems identified during organ transplantation such as surgical restrictions and transplant rejections. Few of these obstacles have been partially removed such as the use of immunosuppressant improved it consistently while decreasing graft rejection up to 12.2%. Methods: This study was conducted from 2019-2021. In all patients renal function was examined through glomerular filtration rate. Induction therapy was given to all the transplant recipients. Induction therapy with basiliximab 20mg intravenously on 0 and 4 days. After transplantation tacrolimus and MMF was given with varied concentration dose. Acute rejections were found in patients who had no biopsy or biopsy-proven rejection. In the end, clinical pathologists had analyzed all biopsies again and recipients who were experienced the vascular Banff grade 2 and tubule interstitial rejection. Results: Immunosuppressant tacrolimus treated patients were 71(67.61%) and mycophenolate mofetil used in 34(32.38%). Total 39(37.14%) rejections were received and 66(62.85%) acceptance was recorded. Two types of rejection were highlighted namely cell-mediated rejection 25(23.80%) and 14(13.33%) chronic antibody-mediated rejection. The effect of tacrolimus on follicular helper T cells and follicular regulatory T cells shows the clear difference between the kidney transplant and healthy control cells. Reduction in numbers of follicular regulatory T cells was measured in patients. Conclusion: eventually we find tacrolimus significantly affects the number of follicular regulatory T-cells and follicular helper T cells. Alemtuzumab substantially lowers the follicular regulatory T-cells. Mycophenolate mofetil showed non-significant on T-cells. Keywords: kidney transplant, follicular regulatory T-cells, follicular helper T-cells.
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26

Eiamsitrakoon, Thanee, Phuntila Tharabenjasin, Noel Pabalan, Hamdi Jarjanazi, and Adis Tasanarong. "Influence of polymorphisms in the vascular endothelial growth factor gene on allograft rejection after kidney transplantation: a meta-analysis." F1000Research 10 (February 10, 2021): 90. http://dx.doi.org/10.12688/f1000research.27800.1.

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Background: Reported associations of allograft rejection in kidney transplant patients with VEGF single nucleotide polymorphisms (SNPs) have been inconsistent between studies, which prompted a meta-analysis to obtain more precise estimates. Methods: Using the PICO elements, kidney transplant patients (P) were compared by genotype data between rejectors (I) and non-rejectors (C) in order to determine the risk of allograft rejection (O) attributed to the VEGF SNPs. Literature search of four databases yielded seven articles. To calculate risks for allograft rejection, four SNPs were examined. Using the allele-genotype model we compared the variant (var) with the wild-type (wt) and heterozygous (var-wt) alleles. Meta-analysis treatments included outlier and subgroup analyses, the latter was based on ethnicity (Indians/Caucasians) and rejection type (acute/chronic). Multiple comparisons were corrected with the Bonferroni test. Results: Five highly significant outcomes (Pa < 0.01) survived Bonferroni correction, one of which showed reduced risk for the var allele (OR 0.61, 95% CI 0.45-0.82). The remaining four indicated increased risk for the wt allele where the chronic rejection (OR 2.10, 95% CI 1.36-3.24) and Indian (OR 1.44, 95% CI 1.13-1.84) subgroups were accorded susceptibility status. Conclusions: Risk associations for renal allograft rejection were increased and reduced on account of the wt and var alleles, respectively. These findings could render the VEGF polymorphisms useful in the clinical genetics of kidney transplantation.
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27

Jutila, Mark A. "Role of changes in the vascular endothelium in chronic inflammation." Clinical Transplantation 8, no. 3pt2 (June 1994): 304–7. http://dx.doi.org/10.1111/j.1399-0012.1994.tb00258.x.

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The recruitment and activation of lymphoid effector cells into grafted tissue is central to the chronic rejection process. The endothelial cells lining inflamed vessels appear to be important in initiating and perpetuating these events through their expression of adhesion proteins for circulating leukocytes, as well as through their production of cytokines and chemokines to attract leukocytes into the inflamed tissues and to activate effector functions. Described here is our current understanding of the role of the vascular endothelium in leukocyte recruitment into inflamed tissues. A model of leukocyte‐endothelial cell interactions is outlined.
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28

Clarke Forbes, R. D., Shu-Xin Zheng, Margaret Gomersall, and Ronald D. Guttmann. "IRREVERSIBLE CHRONIC VASCULAR REJECTION OCCURS ONLY AFTER DEVELOPMENT OF ADVANCED ALLOGRAFT VASCULOPATHY." Transplantation 63, no. 5 (March 1997): 743–49. http://dx.doi.org/10.1097/00007890-199703150-00022.

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29

Shimizu, Tomokazu. "P199 Clinical and pathological analysis of chronic vascular rejection after kidney transplantation." Human Immunology 80 (September 2019): 212. http://dx.doi.org/10.1016/j.humimm.2019.07.252.

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30

O'Hair, Daniel P., Robert P. McManus, and Richard Komorowski. "Inhibition of chronic vascular rejection in primate cardiac xenografts using mycophenolate mofetil." Annals of Thoracic Surgery 58, no. 5 (November 1994): 1311–15. http://dx.doi.org/10.1016/0003-4975(94)91902-x.

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31

Franco-Acevedo, Adriana, Christopher L. Pathoulas, Patrick A. Murphy, and Nicole M. Valenzuela. "The Transplant Bellwether: Endothelial Cells in Antibody-Mediated Rejection." Journal of Immunology 211, no. 9 (November 1, 2023): 1276–85. http://dx.doi.org/10.4049/jimmunol.2300363.

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Abstract Ab-mediated rejection of organ transplants remains a stubborn, frequent problem affecting patient quality of life, graft function, and grant survival, and for which few efficacious therapies currently exist. Although the field has gained considerable knowledge over the last two decades on how anti-HLA Abs cause acute tissue injury and promote inflammation, there has been a gap in linking these effects with the chronic inflammation, vascular remodeling, and persistent alloimmunity that leads to deterioration of graft function over the long term. This review will discuss new data emerging over the last 5 y that provide clues into how ongoing Ab–endothelial cell interactions may shape vascular fate and propagate alloimmunity in organ transplants.
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32

Jonas, S., N. Kling, W. O. Bechstein, G. Blumhardt, R. Lohmann1, H. Lobeck, and P. Neuhaus. "Rejection episodes after liver transplantation during primary immunosuppression with FK506 or a cyclosporine‐based regimen: A controlled, prospective, randomized trial." Clinical Transplantation 9, no. 5 (October 1995): 406–14. http://dx.doi.org/10.1111/j.1399-0012.1995.tb00357.x.

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As part of a European multicenter study to investigate the potency of FK506 in primary immunosuppression after liver transplantation, this comparison with our conventional cyclosporine‐based quadruple regimen was carried out as a controlled, prospective, randomized trial. The 121 patients entering the study were randomly assigned to receive immunosuppressive regimens consisting either of FK506 and prednisolone (FK/n=61) or of cyclosporine, prednisolone, azathioprine, and a 7‐day course of rabbit antithymocyte globulin (CsA/n=60). Rejection was suspected in the case of scant production of light bile or biochemical graft dysfunction, without evidence of vascular, biliary, or infectious complications. A liver biopsy for confirmation of the diagnosis was obtained each time. Initial therapy entailed a 3‐d course of high‐dose methylprednisolone. Steroid resistant rejections were treated with OKT3 monoclonal antibody or, in the group of primary CSA administration, conversion to FK506 as another treatment option. One‐year patient (FK: 90.2%; CsA: 96.7%) and graft survival (FK: 88.5%; CSA: 91.7%) did not differ significantly. Overall, 41 patients (33.9%) experienced 50 acute, cellular rejection episodes (RE) [FK: 25 RE in 21 patients (34.4%); CSA: 25 RE in 20 patients (33.3%)]. The histological grading ranged from mild (FK: 14/25; CSA: 8/25) to moderate (FK: 9/25; CsA: 16/25) and severe (FK: 2/25; CSA: 1/25): not significantly different between the two groups. In the CSA‐based group, three additional rejection episodes were classified as early chronic (n=1) and chronic rejection (n=2). A higher share of late‐onset rejections in the CSA‐group (FK: 1/25, 617d; CsA: 6/25, 164±66d) as well as a more frequently observed occurrence of light bile (FK: 8/25; CsA: 4/25) and overlapping cholangitis (FK: 9/25; CSA: 3/25) in the FK‐group were not significant either. In each group, 10 RE were steroid‐resistant. In the FK‐group, all of them resolved under OKT3; in the CSA‐group, I patient was directly switched to FK506, 6 RE resolved during the OKT3 course, whereas 3 RE were resistant to OKT3. Two OKT3 non‐responders were successfully converted to FK506, the other was suffering from early severe rejection and underwent retransplantation. After another retransplantation for severe hepatitis C reinfection, concomitant findings of chronic rejection type changes were evident and the patient was switched to FK506.These results reflect a comparable low incidence of RE in both groups. Safety in terms of patient and graft survival was high. FK506 as a reported rescue agent seems to hold further potential in reducing late‐onset, ductopenic, and histologically higher‐degree cellular rejections.
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33

Askandarani, Sumayah, Noura Aloudah, Hanan Al Enazi, Khaled O. Alsaad, and Abdulrahman Altamimi. "Late Renal Allograft Rupture Associated with Cessation of Immunosuppression following Graft Failure." Case Reports in Transplantation 2011 (2011): 1–5. http://dx.doi.org/10.1155/2011/512893.

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A 29-year-old man developed chronic allograft nephropathy 63 months after renal transplantation. He became symptomatic with advanced chronic graft failure; his immunosuppressive medications were reduced and he was commenced on haemodialysis. Two months following the withdrawal of immunosuppression, he presented with abdominal pain, haematuria, and a marked drop in haemoglobin. The patient was taken to the operating room, where the renal allograft was found to be ruptured, and graft nephrectomy was subsequently performed. Histological examination of the graft specimen showed severe haemorrhagic acute vascular cellular rejection in a background of marked chronic allograft vasculopathy. Immunostaining for C4d showed diffuse, strong, linear circumferential staining of the peritubular capillaries, indicating a concurrent antibody-mediated rejection. We report herein an unusual case of spontaneous renal allograft rupture that occurred long time after transplantation due to severe acute rejection following cessation of immunosuppressive medications for advanced chronic allograft failure. To the best of our knowledge, the time interval between transplantation and the rupture of this allograft is the longest of those reported in the literature.
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34

Orosz, Charles G. "Endothelial activation and chronic allograft rejection." Clinical Transplantation 8, no. 3pt2 (June 1994): 299–303. http://dx.doi.org/10.1111/j.1399-0012.1994.tb00257.x.

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Microvascular endothelial cells are actively involved in acute and hyperacute allograft rejection. In acute rejection, inflamed graft endothelia increase their expression of cell adhesion and antigen‐presentation molecules, thereby initiating and promoting various mechanisms of cellular immune rejection. In hyperacute rejection, preformed antibodies bind to graft endothelial cells and initiate endothelial procoagulant activity. These disparate immune responses appear to reflect different manifestations of endothelial cell activation. We hypothesize that chronic allograft rejection is a third manifestation of local endothelial activation. Chronic rejection is associated with interstitial and/or vascular hypertrophy. It is intriguing that among the products of activated endothelial cells are extracellular matrix components and growth factors that promote tissue reconstruction. This suggests that chronic or repetitive stimulation of endothelial cells may cause persistent or periodic release of these growth factors, eventually leading to the histopathology of chronic rejection. Chronic endothelial stimulation could be accomplished by drugs, alloantibodies, immune mediators, or some combination thereof. This leads to the question: Do different patterns of endothelial stimulation result in different manifestations of endothelial activation? Our studies of acute rejection mechanisms in murine cardiac allografts demonstrated that several stable endothelial phenotypes can develop during graft inflammation, depending on the availability of local immune stimuli (Transplantation 1993: 55: 315). Unpublished studies suggest that the steroids prednisolone and dexamethasone can synergize in vitro with suboptimal concentrations of interferon‐gamma (IFN‐γ) to promote the activation of human endothelial cell lines, as manifested by enhanced expression of MHC class II but not ICAM‐1. These steroids do not influence tumor necrosis factor‐alpha (TNF‐α)‐induced endothelial behavior. Yet to be determined is whether this drug and cytokine combination influences the production of growth factors by endothelia. Transplant recipients receive steroids for maintenance immunosuppression; IFN‐γ could be produced by random immune responses to environmental antigens, thus resulting in chronic endothelial stimulation in graft recipients. Finally, our lab and others have observed that a component of scrum from some high PRA (panel‐ reactive antibody) patients can activate cultured, human endothelial cells, as manifested by heightened ICAM‐1 expression. Other parameters of endothelial activation have not yet been investigated in this way. We have noted that endothelial cells arc relatively difficult to kill with antibody and complement, but that they can be activated through their receptors for products of the complement cascade. It remains to be determined whether serum from individuals with ongoing chronic rejection also can mediate this effect, or promote endothelial growth factor production. In sum, there is evidence that endothelial cells can be activated by a variety of immune and physiologic stimuli, and that the outcome of endothelial activation varies widely and depends on the combination of stimuli present, thus influencing the pattern of subsequent histopathology at the inflammatory site. This supplies the groundwork for the hypothesis that chronic allograft rejection may be a manifestation of local endothelial activation by a particular combination of physiologic, immunologic and pharmacologic stimuli.
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35

Zlabinger, Gerhard J., Walter Ulrich, Martin Pecherstorfer, Bruno Watschinger, Otto Traindl, Giora Meron, Erich Pohanka, Johanna Wolfram, and Josef Kovarik. "Clinical experience with OKT3 monoclonal antibody for treatment of acute renal allograft rejection based on sequential histological evaluation." Clinical Transplantation 3, no. 4 (August 1989): 215–22. http://dx.doi.org/10.1111/j.1399-0012.1989.tb00185.x.

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Based on sequential histological evaluation, monoclonal antibody treatment with OKT3 was able to reverse 25 out of 34 (74%) acute rejection episodes treated as first line but only 6 out of 15 (40%) acute rejection episodes treated on a rescue basis in renal transplant recipients. Within the histologically‐defined responder group to OKT3, 25% of the treated patients did not show an improvement of excretory kidney function during or immediately after monoclonal antibody treatment and these were significantly more frequent in the patient group with late acute interstitial rejection. In these patients clinically unapparent chronic cyclosporine‐A nephrotoxicity seemed to have been aggravated by the rejection process so that excretory kidney function did not recover after effective treatment of rejection. Actual graft function 3 to 27 months after initiation of OKT3 therapy was significantly worse in nonresponders than in responders (p<0.001). Significantly more patients not responding to OKT3 therapy were found in the group of graft recipients with no initial transplant function (p = 0.03). Vascular components and signs of severe interstitial acute rejections were the predominant histological lesions in non‐responders to OKT3. A strong correlation could be found between the incidence of both CMV and viral infections in general and the duration of the OKT3 treatment cyclus (p = 0.01). Our findings confirm that OKT3 is effective in reversing acute renal allograft rejection and, additionally, provide evidence that differential indications for OKT3 therapy might exist that may help to maximize control of rejection and to avoid unnecessary side effects due to inadequate courses of treatment.
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36

Subbotin, V. M., J. L. Tang, M. A. Antonysamy, A. B. Troutt, A. S. Rao, and A. W. Thomson. "AN IL-17 RECEPTOR ANTAGONIST INHIBITS THE PATHOGENESIS OF ACUTE VASCULAR REJECTION BUT NOT DEVELOPMENT OF CHRONIC REJECTION." Transplantation 69, Supplement (April 2000): S195. http://dx.doi.org/10.1097/00007890-200004271-00313.

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37

Dunning, J. E., N. Chin, G. Westall, G. Snell, and C. A. McLean. "Chronic vascular rejection - a common finding in the lung allograft is associated with features of antibody mediated rejection." Pathology 46 (2014): S63. http://dx.doi.org/10.1097/01.pat.0000443546.50411.60.

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38

Song, Ethan Y., Brooke E. Barrow, and Linda C. Cendales. "Vascular changes in vascularized composite allotransplantation." Current Opinion in Organ Transplantation 29, no. 6 (November 1, 2024): 363–67. http://dx.doi.org/10.1097/mot.0000000000001184.

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Purpose of review Allograft vasculopathy in vascularized composite allografts (VCA) remains understudied. This review explores the vascular changes in VCA, focused on recent literature. Recent findings Allograft vasculopathy in VCA generally includes progressive concentric myointimal thickening and luminal narrowing of arterial vessels through endothelial deterioration and proliferation of smooth muscle cells. Microvascular changes are also noted, with thrombosis and lumen narrowing in microvessels of the skin even in the absence of large vessel vasculopathy. Histopathologic reports of skin containing VCA rejection document arteriosclerosis in deep vessels that are not always reflected in skin punch biopsies. The first revision of the Banff VCA scoring system 2022 was developed to include vascular changes in VCA. The scoring system for chronic changes and antibody mediated rejection continues to be under development. Summary The study of vascular changes in VCA continues to progress. Important data and advances in experimental and clinical VCA have been reported and continue to take place. Challenges ahead include capture of clinical data that will evolve beyond transient report forms and approaching on the problem of graft failure well grounded in sound scientific methodology.
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39

Parizhskaya, Maria, Clara Redondo, Anthony Demetris, Ronald Jaffe, Jorge Reyes, Kris Ruppert, Lillian Martin, and Kareem Abu-Elmagd. "Chronic Rejection of Small Bowel Grafts: Pediatric and Adult Study of Risk Factors and Morphologic Progression." Pediatric and Developmental Pathology 6, no. 3 (May 2003): 240–50. http://dx.doi.org/10.1007/s10024-002-0039-4.

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One hundred and seventy-two patients underwent small bowel transplantation at Children's Hospital of Pittsburgh and University of Pittsburgh Medical Center between May 1990 and August 2001. Thirty-four patients had complete or partial resection of their primary graft and in 15, histologic features of chronic rejection were present in the resected small bowel. This is a descriptive and correlative study of the demographic, perioperative, and histologic features associated with progression to intestinal graft failure. Variable features associated with an increased risk of chronic rejection included acute rejection within the 1st month, increased number and higher grade of acute rejection episodes, isolated small bowel grafts rather than small bowel–liver grafts, older recipient age, non-Caucasian race, and Caucasian to non-Caucasian transplant. The mucosal biopsies showed predictive changes many months before the grafts were excised. The mucosal biopsy diagnosis of chronic vascular rejection can be difficult because the affected vessels, the distal branches of the mesenteric arteries, and the larger arteries of the subserosa and submucosa are not routinely sampled. The possibility of underlying arteriopathy, however, can be inferred in some instances from the presence of secondary mucosal changes in the small bowel biopsies though the “early” changes lack specificity. It is the progression of biopsy findings over time that is predictive of outcome. It is important to recognize the persistence of “late” mucosal changes of chronic rejection so that patients are not subjected to increased immune suppression when it is unlikely to be of significant benefit.
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40

Simic-Ogrizovic, Sanja, Angelina Starcevic-Bozovic, Radmila Blagojevic, Dragana Radivojevic, and Ljubica Djukanovic. "PCNA in assessment of progression rate of chronic renal allograft rejection." Srpski arhiv za celokupno lekarstvo 130, no. 5-6 (2002): 159–64. http://dx.doi.org/10.2298/sarh0206159s.

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Chronic graft failure may occur due to CR, cyclosporine nephrotoxicity repeated acute rejection, recurrent glomerular diseases, surgical and urological complications, but CR was recognized as the most common cause of chronic graft failure and renal graft loss [7]. Progression of renal disease reflects the interactive effects of changes in the structure and function. This notion has been examined many times in the native kidneys by studies correlating glomerular filtration rate with architectural deterioration in the glomerular or interstitial compartment [8-10]. Meanwhile, the similar studies in human renal allograft are scarce. Increased PCNA immunodetection in glomerular cells as well as in interstitial infiltrates was described in acute and chronic renal graft rejection and diagnostic value of this finding was analyzed [12,15]. Similarly, PCNA was often examined immunohistochemically in lymphoma and solid tumors as a marker of cell proliferation, but its reliability as a prognostic factor was also evaluated [18-20]. In the present study the prognostic value of PCNA expression in different tissue compartments of renal grafts experiencing CR was examined for the first time. The present study revealed that two groups examined with the different chronic graft failure progression rate as the main difference had significantly different proliferation of cells in glomerular, TIN and vascular compartments. PCNA immunoreactivity scores in these three compartments were significantly higher in the fast than in slow progression group. The significant positive correlation between the slope of the regression line plotting 1/sCr vs. time and cell proliferation in glomerular, TIN and vascular compartments was also found. Therefore, it was suggested that the measurement of PCNA expression in renal graft tissue might be used as a prognostic index.
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41

Oguma, Shiro, T. Zerbe, B. Banner, Thomas Starzl, and A. J. Demetris. "PARTICIPATION OF DENDRITIC CELLS IN VASCULAR LESIONS OF CHRONIC REJECTION OF HUMAN ALLOGRAFTS." Lancet 332, no. 8617 (October 1988): 933–36. http://dx.doi.org/10.1016/s0140-6736(88)92600-1.

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42

Martelius, Timi, Leena Halme, Johanna Arola, Krister Höckerstedt, and Irmeli Lautenschlager. "Vascular deposition of complement C4d is increased in liver allografts with chronic rejection." Transplant Immunology 21, no. 4 (September 2009): 244–46. http://dx.doi.org/10.1016/j.trim.2009.06.004.

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43

Srivastava, R., M. Curtis, S. Hendricks, W. Burns, and J. D. Hosenpud. "CMV STRAIN-SPECIFIC ALTERATIONS INDUCED IN VASCULAR ENDOTHELIAL CELLS: IMPLICATIONS FOR CHRONIC REJECTION." Transplantation 67, no. 7 (April 1999): S52. http://dx.doi.org/10.1097/00007890-199904150-00212.

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44

Ghasemian, Seyed R., Jimmy A. Light, Charles B. Currier, Truman Sasaki, Alex Aquino, John Rees, William Ward, and James Carr. "The significance of the IgG anti‐B‐cell crossmatch on renal transplant outcome." Clinical Transplantation 11, no. 5pt2 (October 1997): 485–87. http://dx.doi.org/10.1111/j.1399-0012.1997.tb01029.x.

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Transplantation in the presence of anti‐class I antibodies usually results in allograft hyperacute rejection. Because of the perception of its uncertain clinical significance, B‐cell crossmatch which identifies presence of anti‐class II antibodies is not universally performed. In a retrospective study, the clinical course of renal transplant recipients with IgG anti‐B‐cell antibodies was analyzed and compared with case control patients transplanted contemporaneously, matched demographically and immunologically. The incidence of hyperacute, acute, and chronic rejection as well as graft loss were significantly higher in the group with anti‐IgG B‐cell antibodies compared to the control. We conclude that anti‐B‐cell IgG antibodies are harmful to allografts with a spectrum of events that include hyperacute, acute, vascular and chronic rejection. While allografts were successful in some patients, our experience suggests caution whenever anti‐donor B‐cell IgG is present. If transplants are performed, then more potent immunosuppression should be used.
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45

Hegeman, Rebecca L., and Lawrence G. Hunsicker. "Chronic rejection in renal allografts: importance of cardiovascular risk factors." Clinical Transplantation 9, no. 2 (April 1995): 135–39. http://dx.doi.org/10.1111/j.1399-0012.1995.tb00312.x.

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Using a case‐control method, we reviewed retrospectively renal transplants performed at University of Iowa Hospitals & Clinics between April 1, 1973 and May 29, 1991 to see if cardiovascular risk factors such as obesity, blood pressure, cholesterol, and tobacco use were important risk factors for development of chronic vascular rejection. Of 1161 transplants done during that time, 834 patients had renal allografts which functioned for greater than 365 days. From this subgroup we selected all surviving patients (n=97) who had a functioning graft for greater than 365 days but whose graft subsequently failed. We also selected all patients (n=26) who died with a functioning graft. Finally, we selected 52 control patients who were still living with functioning grafts, approximately matched to the study patients for date of transplant. We found no significant difference among the three groups in weight and weight changes, mean blood pressures, mean serum cholesterol values, or tobacco use. Our findings agree with previously published studies indicating a lack of correlation of cardiovascular risk factors with the development of chronic rejection of renal allografts in humans.
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46

Noguchi, Shin-ichi, Jorge Reyes, George V. Mazariegos, Maria Parizhskaya, and Ronald Jaffe. "Pediatric Intestinal Transplantation: The Resected Allograft." Pediatric and Developmental Pathology 5, no. 1 (January 2002): 3–21. http://dx.doi.org/10.1007/s10024-001-0140-0.

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We reviewed the clinical and pathologic finding of 22 resected allografts from 19 of the 83 children who underwent a variety of small intestinal transplant procedures in the years 1990–2000 at the Children's Hospital of Pittsburgh. Resections were compared with prior mucosal biopsies because resections allow for evaluation of the entire bowel thickness, including the feeding vessels, and obviate the problems of limited sampling. Partial resections that were done soon after the transplant, or soon after additional surgery, were for surgical problems such as leaks, adhesions, and volvulus. None had biopsy features suggestive of rejection or infection. Partial resections done late (6 months or more) after transplantation were more likely to be related to allograft immune biology; two had a sclerosing peritonitis that was confined to the allograft, and one had an obstructing carcinoma arising in the allograft mucosa. One patient had a localized stricture, demonstrated to be due to graft vascular disease at partial resection, and this patient went on to have the allograft removed a year later for chronic rejection. Early complete allograft enterectomies were for refractory acute cellular rejection, 1–2 months following transplant. One was removed for pancreatitis and liver failure from operative complications. Late allograft enterectomies were generally for chronic rejection, some with residual acute rejection, but there were also a number of patients who had multiple superimposed conditions such as cytomegalovirus, Epstein-Barr virus, and post-transplant lymphoproliferative disorder in various combinations. One had idiopathic scarring and developed an adynamic bowel that remains unexplained. Examination of the resected specimens allows for dissection of the multiple contributions to graft failure, especially the vascular disease that can rarely be seen on mucosal biopsy. An unexpected finding was the impressive hypertrophy of neural elements, nerves, and ganglion cells in many of the patients, the significance of which requires further investigation.
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47

Bian, Hong, and Elaine F. Reed. "Alloantibody-Mediated Class I Signal Transduction in Endothelial Cells and Smooth Muscle Cells: Enhancement by IFN-γ and TNF-α." Journal of Immunology 163, no. 2 (July 15, 1999): 1010–18. http://dx.doi.org/10.4049/jimmunol.163.2.1010.

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Abstract Chronic rejection is the major limiting factor to long term survival of solid organ allografts. The hallmark of chronic rejection is transplant atherosclerosis, which is characterized by the intimal proliferation of smooth muscle cells, endothelial cells, and fibroblasts, leading to vessel obstruction, fibrosis, and eventual graft loss. The mechanism of chronic rejection is poorly understood, but it is suspected that the associated vascular changes are a result of anti-HLA Ab-mediated injury to the endothelium and smooth muscle of the graft. In this study we have investigated whether anti-HLA Abs, developed by transplant recipients following transplantation, are capable of transducing signals via HLA class I molecules, which stimulate cell proliferation. In this report we show that ligation of class I molecules with Abs to distinct HLA-A locus and HLA-B locus molecules results in increased tyrosine phosphorylation of intracellular proteins and induction of fibroblast growth factor receptor expression on endothelial and smooth muscle cells. Treatment of cells with IFN-γ and TNF-α up-regulated MHC class I expression and potentiated anti-HLA Ab-induced fibroblast growth factor receptor expression. Engagement of class I molecules also stimulated enhanced proliferative responses to basic fibroblast growth factor, which augmented endothelial cell proliferation. These findings support a role for anti-HLA Abs and cytokines in the transduction of proliferative signals, which stimulate the development of myointimal hyperplasia associated with chronic rejection of human allografts.
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48

Mallek, R., G. H. Mostbeck, R. Kain, G. Sunder-Plassmann, T. Helbich, and D. Tscholakoff. "Polyetiology of Renal Allograft Dysfunction." Acta Radiologica 33, no. 5 (September 1992): 434–39. http://dx.doi.org/10.1177/028418519203300511.

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In 101 consecutive patients with renal allograft dysfunction a correlation of Duplex Doppler sonography (DDS) with histopathologic reports of simultaneously performed biopsies was made. Renal vascular impedance was estimated by calculating the resistive index (RI). A total of 290 different specific histologic diagnoses (mean 2.1 ± 0.84 diagnoses/biopsy) was noted. With increasing time interval to transplantation, single diagnoses as cause of allograft dysfunction decreased. DDS could not reliably differentiate, exclude, or grade any of the common causes of renal allograft dysfunction like vascular and/or cellular rejection, chronic rejection, acute tubular necrosis, cyclosporin nephrotoxicity, relapse of glomerulonephritis and infection. Follow-up studies after established histologic diagnosis in 19 patients with persisting allograft dysfunction demonstrated a lack of sensitivity of DDS to significant superimposed causes of transplant malfunction. We conclude that biopsy is still necessary to direct proper therapy of renal allograft dysfunction.
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49

Libby, Peter, and Hiroyuki Tanaka. "The pathogenesis of coronary arteriosclerosis (“chronic rejection”) in transplanted hearts." Clinical Transplantation 8, no. 3pt2 (June 1994): 313–18. http://dx.doi.org/10.1111/j.1399-0012.1994.tb00260.x.

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“Chronic rejection” of allografts may mean different things to different people. Some use this term to refer to a process more specifically described as arteriosclerotic obstruction of the coronary arteries of transplanted hearts. A number of mechanisms might contribute to the pathogenesis of this accelerated form of arterial disease, including administration of immunosuppressive agents such as corticosteroids with attendant hyperlipoproteinemia, viral infections, or ischemic injury of coronary artery endothelium occurring between harvest and reimplantation. However, involvement of the engrafted vessels with sparing of the host's native arteries suggested to us that immune phenomena underlie graft arteriosclerosis. In 1989 we proposed a model for the pathogenesis of accelerated arteriosclerosis associated with cardiac transplantation that linked a cellular immune response akin to delayed‐type hypersensitivity to leukocyte recruitment and altered vascular cell function via a cytokine cascade (1). In support of this concept, coronary artery endothelium can express class II histocompatibility antigens (HLA) that might elicit a cellular immune response (2, 3). Leukocytes including macrophages and T lymphocytes accumulate in transplanted coronary arteries, as would be expected if an ongoing immune or inflammatory response contributed to this type of “chronic rejection”. As we have previously suggested, T cells activated by graft endothelial cells that bear class II HLA probably secrete cytokines that could promote macrophage recruitment and activation, and proliferation and extracellular matrix synthesis by smooth muscle cells. Adhesion molecule expression by vascular cells may participate not only in recruitment and retention of leukocytes but also may promote immune responses by providing co‐stimulating or accessory function to T cells as well. We and others have noted a striking localization of T lymphocytes in an annular distribution just under the luminal endothelium in coronary arteries from transplanted hearts. This array of T lymphocytes immediately subjacent to the class II‐bearing endothelial cells suggests a localized allogeneic immune response in such vessels. Arteriosclerotic lesions in the coronary arteries of transplanted hearts contain increased levels of the cytokine monocyte‐chemoattractant and activating protein‐1 (MCP)‐1 (4). These data support the hypothesis that transplantation arteriosclerosis involves a cytokine cascade triggered by. and contributing to, a chronic cellular immune response. However, other mechanisms or combinations of various inciting factors may play a role in this process. Ultimately, experimental strategies that test various specific immunopathologic mechanisms will be required to ferret out their contributions to the development of this form of arteriosclerosis. Observations on human tissues, when available, will complement and test the clinical relevance of studies in experimental animals. It will be useful to distinguish various specific types of immune injury that could involve allografted vessels as we struggle to define our terms more precisely and arrange the pieces of the puzzle of the pathogenesis of transplantation‐associated arteriosclerosis in some logical order. The schema within represents an oversimplified attempt in this direction.
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50

Dorling, Anthony, and Robert I. Lechler. "Xenotransplantation: Immune Barriers beyond Hyperacute Rejection." Clinical Science 93, no. 6 (December 1, 1997): 493–505. http://dx.doi.org/10.1042/cs0930493.

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1. The use of organs from animal donors (xenotransplantation) is a potential solution to the chronic shortage of allogeneic organs and currently the pig is thought to be the most suitable donor for man. However, porcine organs are rejected rapidly by a vascular process called hyperacute rejection which has so far prevented clinical xenotransplantation. Although it is likely that this barrier will be overcome in the near future by the application of novel strategies, probably involving the use of organs from transgenic pigs, data from animal models indicate that multiple other immune mechanisms will contribute to the rejection of xenografts. 2. We have described two aspects of these immune mechanisms. First, the phenomenon of ‘accommodation’, whereby xenografts acquire in vivo resistance to vascular rejection, has been explored in an in vitro model utilizing immortalized porcine endothelial cells. The results indicate that human anti-pig antibodies induce a concentration-dependent and time-dependent change in porcine endothelial cells compatible with the development of accommodation. 3. Secondly, the in vitro human anti-porcine T-cell response has been documented in detail, with particular emphasis on quantitative and qualitative comparisons with the in vitro T-cell alloresponse. The results of this work, which indicate that the response to porcine xenografts is likely to be significantly stronger than that against allografts, have important implications for the level of conventional immunosuppression that may be necessary to prevent xenograft rejection, and provide an important basis for the development of strategies to promote xenograft-specific immunosuppression and tolerance.
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