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Journal articles on the topic 'Cellular rejection'

Author: Grafiati

Published: 4 June 2021

Last updated: 26 April 2022

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1

Willicombe, Michelle, Candice Roufosse, Paul Brookes, Adam G. McLean, Jack Galliford, Tom Cairns, Terry H. Cook, and David Taube. "Acute Cellular Rejection." Transplantation Journal 97, no. 4 (February 2014): 433–39. http://dx.doi.org/10.1097/01.tp.0000437431.97108.8f.

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2

Wecker, Hermann, and Hugh Auchincloss. "Cellular mechanisms of rejection." Current Opinion in Immunology 4, no. 5 (January 1992): 561–66. http://dx.doi.org/10.1016/0952-7915(92)90026-b.

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3

Korsgren, Olle. "Acute cellular xenograft rejection." Xenotransplantation 4, no. 1 (February 1997): 11–19. http://dx.doi.org/10.1111/j.1399-3089.1997.tb00159.x.

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4

Subherwal, S., J. A. Kobashigawa, G. Cogert, J. Patel, M. Espejo, and B. Oeser. "Incidence of acute cellular rejection and non-cellular rejection in cardiac transplantation." Transplantation Proceedings 36, no. 10 (December 2004): 3171–72. http://dx.doi.org/10.1016/j.transproceed.2004.10.048.

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5

Bolton, E. M., J. A. Gracie, J. D. Briggs, J. Kampinga, and J. A. Bradley. "Cellular requirements for renal allograft rejection in the athymic nude rat." Journal of Experimental Medicine 169, no. 6 (June 1, 1989): 1931–46. http://dx.doi.org/10.1084/jem.169.6.1931.

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This study has examined the ability of adoptively transferred CD4+ and CD8+ T cells to mediate rejection of a fully allogeneic DA renal graft in the PVG nude rat. Transfer, at the time of transplantation, of naive CD4+ T cells caused rapid graft rejection and primed CD4+ cells were several times more potent. In contrast, naive or specifically sensitized CD8+ cells were entirely ineffective at mediating renal allograft rejection. Whereas nonrejecting grafts showed only a mild cellular infiltrate, rejecting grafts in CD4+ reconstituted animals showed a substantial infiltrate and many of the infiltrating cells had a phenotype (MRC OX8+, MRC OX19-), consistent with NK cells. Experiments using a mAb (HIS 41) against an allotypic determinant of the leukocyte common antigen confirmed that the majority (greater than 80%) of the cellular infiltrate in rejecting grafts derived from the host rather than from the CD4+ inoculum. Infiltrating mononuclear cells, obtained from rejecting allografts 7 d after transplantation in CD4+-injected PVG nude hosts, showed high levels of in vitro cytotoxicity against not only kidney donor strain Con A blasts but also third-party allogeneic Con A blasts, as well as against both NK and LAK susceptible targets. When splenocytes from nontransplanted nude PVG rats were tested in vitro they also demonstrated high levels of lytic activity against both NK and LAK susceptible targets as well as allogeneic Con A blasts, which were not susceptible to lysis by spleen cells from euthymic rats. These findings suggest that injected CD4+ cells may cause renal allograft rejection by the recruitment of extrathymically derived, widely alloreactive cells into the kidney in this model of graft rejection.

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6

Pinchuk, A. V., R. V. Storozhev, I. V. Dmitriev, N. V. Shmarina, G. A. Nefedova, R. Sh Muslimov, and Yu S. Teterin. "Cellular rejection of pancreaticoduodenal graft." Russian Journal of Transplantology and Artificial Organs 20, no. 3 (September 17, 2018): 80–86. http://dx.doi.org/10.15825/1995-1191-2018-3-80-86.

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Aim. The evaluation of donor’s duodenum histological examination in diagnosis of pancreaticoduodenal graft rejection.Materials and methods. The 35-yo patient with terminal diabetic nephropathy undergone simultaneous retroperitoneal kidney and pancreas transplantation with enteric exocrine drainage of the graft via inter-duodenal anastomosis. When performing the esophagogastroduodenoscopy 2 years posttransplant we implemented histologic examination of the duodenum of the graft.Results. We diagnosed and verified severe cellular rejection of pancreaticoduodenal graft. Successful etiopathogenetic treatment of acute rejection of the graft (pulse therapy with glucocorticoids) was performed.Discussion. The diagnostic value of donor’s duodenum morphological examination in the diagnosis of pancreaticoduodenal graft rejection, the efficacy of anti-rejection treatment were performed in this case.

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7

Hutchinson, Ian V. "Cellular mechanisms of allograft rejection." Current Opinion in Immunology 3, no. 5 (October 1991): 722–28. http://dx.doi.org/10.1016/0952-7915(91)90103-8.

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8

Nikaein, Afzal. "Cellular Basis of Allograft Rejection." Baylor University Medical Center Proceedings 1, no. 2 (April 1988): 39–48. http://dx.doi.org/10.1080/08998280.1988.11929670.

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9

Hamdorf, Matthias, Satoru Kawakita, and Matthew Everly. "The Potential of MicroRNAs as Novel Biomarkers for Transplant Rejection." Journal of Immunology Research 2017 (2017): 1–12. http://dx.doi.org/10.1155/2017/4072364.

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The control of gene expression by microRNAs (miRNAs, miR) influences many cellular functions, including cellular differentiation, cell proliferation, cell development, and functional regulation of the immune system. Recently, miRNAs have been detected in serum, plasma, and urine and circulating miR profiles have been associated with a variety of diseases. Rejection is one of the major causes of allograft failure and preventing and treating acute rejection are the central task for clinicians working with transplant patients. Invasive biopsies used in monitoring rejection are burdensome and risky to transplant patients. Novel and easily accessible biomarkers of acute rejection could make it possible to detect rejection earlier and make more fine-tuned calibration of immunosuppressive or new target treatment possible. In this review, we discuss whether circulating miRNA can serve as an early noninvasive diagnostic biomarker and an expression fingerprint of allograft rejection and transplant failure. Understanding the regulatory interplay of relevant miRNAs and the rejecting allograft will result in a better understanding of the molecular pathophysiology of alloimmune injury.

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10

Manyeruke, F., T. Pennel, R. Roberts, and G. L. Calligaro. "Acute cellular rejection in lung transplantation." African Journal of Thoracic and Critical Care Medicine 25, no. 2 (July 31, 2019): 55. http://dx.doi.org/10.7196/sarj.2019.v25i2.010.

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11

Wada, S., H. Ochikubo, Y. Sugawara, T. Sueda, K. Fujii, H. Kajihara, and Y. Matsuura. "Cellular immune reaction in hyperacute rejection." Transplantation Proceedings 30, no. 7 (November 1998): 3818–20. http://dx.doi.org/10.1016/s0041-1345(98)01250-0.

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12

Charlton, Michael R. "How important is acute cellular rejection?" Liver Transplantation 19, S2 (October 24, 2013): S9—S13. http://dx.doi.org/10.1002/lt.23743.

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13

Ingulli, Elizabeth. "Mechanism of cellular rejection in transplantation." Pediatric Nephrology 25, no. 1 (January 2010): 61–74. http://dx.doi.org/10.1007/s00467-008-1020-x.

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14

Emmerich, Florian, Stefan Zschiedrich, Christine Reichenbach-Braun, Caner Süsal, Susana Minguet, Marie-Christin Pauly, and Maximilian Seidl. "Low Pre-Transplant Caveolin-1 Serum Concentrations Are Associated with Acute Cellular Tubulointerstitial Rejection in Kidney Transplantation." Molecules 26, no. 9 (April 30, 2021): 2648. http://dx.doi.org/10.3390/molecules26092648.

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Acute and chronic transplant rejections due to alloreactivity are essential contributors to graft loss. However, the strength of alloreactivity is biased by non-immunological factors such as ischemia reperfusion injury (IRI). Accordingly, protection from IRI could be favorable in terms of limiting graft rejection. Caveolin-1 (Cav-1) is part of the cell membrane and an important regulator of intracellular signaling. Cav-1 has been demonstrated to limit IRI and to promote the survival of a variety of cell types including renal cells under stress conditions. Accordingly, Cav-1 could also play a role in limiting anti-graft immune responses. Here, we evaluated a possible association between pre-transplant serum concentrations of Cav-1 and the occurrence of rejection during follow-up in a pilot study. Therefore, Cav-1-serum concentrations were analyzed in 91 patients at the time of kidney transplantation and compared to the incidence of acute and chronic rejection. Higher Cav-1 levels were associated with lower occurrence of acute cellular tubulointerstitial rejection episodes.

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15

Orandi, B., E. Kraus, S. Bagnasco, K. Van Arendonk, J. Garonzik-Wang, R. Montgomery, and D. Segev. "Outcomes of Concurrent Cellular Rejection in Patients With Antibody-Mediated Rejection." Transplantation 98 (July 2014): 436. http://dx.doi.org/10.1097/00007890-201407151-01443.

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16

Antończyk, K., M. Zakliczynski, R. Antończyk, M. Zembala, and T. Kukulski. "Strain Rejection Score to Diagnose Acute Cellular Rejection After Heart Transplantation." Journal of Heart and Lung Transplantation 36, no. 4 (April 2017): S233—S234. http://dx.doi.org/10.1016/j.healun.2017.01.617.

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17

Honsova, E., A. Lodererova, P. Balaz, and M. Oliverius. "Plasma citrulline levels and acute cellular rejection early after small bowel transplantation in pigs." Veterinární Medicína 54, No. 5 (June 1, 2009): 215–22. http://dx.doi.org/10.17221/47/2009-vetmed.

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Small bowel transplantations (SBT) are increasingly performed to treat patients with irreversible intestinal failure or short-bowel syndrome. Histologic evaluation of small bowel allograft biopsies is important for the diagnosis of acute cellular rejection (ACR). A reliable serological marker of ACR after SBT is still unknown. Recently, citrulline was identified as a potential biomarker of reduced enterocyte mass. The aim of our study was to analyze rejection and plasma citrulline levels early after SBT in pigs. 24 pigs were used and divided into four groups. Group A, autologous SBT (<I>n</I> = 3) as a control group; Group B, allogeneic SBT with tacrolimus monotherapy (<I>n</I> = 7); Group C, allogeneic SBT immunosuppressed with tacrolimus and sirolimus (<I>n</I> = 8); and Group D, without immunosuppresion (<I>n</I> = 6). The observation period was 30 days. Mucosal biopsies were obtained on Days 0, 3, 5, 7, 10, 14, 20, 28 and simultaneously plasma citrulline levels were measured. ACR was classified according to standardized grading schema on a scale of indeterminate, mild, moderate, and severe. There were no significant differences in citrulline plasma levels between cases with mild ACR and indeterminate for ACR. A significant decline in plasma citrulline levels occurred in cases of moderate and severe rejection. Plasma citrulline levels constituted a marker of more advanced injury of small bowel epithelium.

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18

Cogert, G. A., S. Subherwal, G. Wu, J. K. Patel, M. Espejo Vassilakis, M. C. Fishbein, J. Moriguchi, H. Laks, and J. A. Kobashigawa. "Incidence of non-cellular (humoral) rejection unchanged in the 1990 decade despite a decrease in cellular rejection." Journal of Heart and Lung Transplantation 22, no. 1 (January 2003): S119—S120. http://dx.doi.org/10.1016/s1053-2498(02)00837-9.

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19

Dogan, Nurettin, Anna Hüsing-Kabar, Hartmut H. Schmidt, Vito R. Cicinnati, Susanne Beckebaum, and Iyad Kabar. "Acute allograft rejection in liver transplant recipients: Incidence, risk factors, treatment success, and impact on graft failure." Journal of International Medical Research 46, no. 9 (July 12, 2018): 3979–90. http://dx.doi.org/10.1177/0300060518785543.

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Objective This study was performed to identify risk factors for acute cellular rejection after liver transplantation (LT). Methods Consecutive LT recipients who underwent surgery in our institution from 2002 to 2015 were retrospectively evaluated. Results In total, 176 patients were eligible for statistical analysis. During a mean observation period of 61.1 ± 36.3 months, 43 episodes of acute rejection were evident. Of these, 34 (79.0%) were responsive to methylprednisolone, 3 (7.0%) were treated by adjusting the dosage of immunosuppressive agents, and 6 (14.0%) were methylprednisolone-resistant and treated using anti-thymocyte globulin. Biliary complications (odds ratio [OR] = 4.89, 95% confidence interval [CI] = 2.00–11.98); donor-negative, recipient-positive CMV mismatch (OR = 9.88, 95% CI = 1.18–82.36); sex mismatch (OR = 3.16, 95% CI = 1.31–8.10); and sex mismatch with a female donor (OR = 3.00, 95% CI = 1.10–7.58) were identified as significant risk factors for acute graft rejection after LT. Conclusion In patients who develop acute cellular rejection after LT, biliary complications should be evaluated as a potential cause. Most acute rejections after LT respond to bolus corticosteroid therapy.

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20

Dullens, H. F. J., S. Schakenrad, and W. Den Otter. "Spontaneous tumor rejection is not always due to a complete cellular rejection." Experimental pathology 31, no. 1 (January 1987): 33–38. http://dx.doi.org/10.1016/s0232-1513(87)80090-7.

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21

Mandel, T. E., J. Kovarik, M. Koulmanda, and H. M. Georgiou. "Cellular rejection of fetal pancreas grafts: Differences between alio- and xenograft rejection." Xenotransplantation 4, no. 1 (February 1997): 2–10. http://dx.doi.org/10.1111/j.1399-3089.1997.tb00158.x.

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22

Goekler, J., A. Zuckermann, E. Osorio, K. Uyanik-Uenal, G. Laufer, and A. Aliabadi-Zuckermann. "Acute Cellular Rejection (ACR) ± Antibody Mediated Rejection (AMR) - Double Trouble or Overrated?" Journal of Heart and Lung Transplantation 36, no. 4 (April 2017): S223. http://dx.doi.org/10.1016/j.healun.2017.01.586.

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23

Rose, Marlene L. "Understanding the Mechanisms of Acute Cellular Rejection." Graft 4, no. 1 (January 2001): 57–59. http://dx.doi.org/10.1177/152216280100400115.

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24

Koutsokera, Angela, Liran Levy, Prodipto Pal, Ani Orchanian-Cheff, and Tereza Martinu. "Acute Cellular Rejection: Is It Still Relevant?" Seminars in Respiratory and Critical Care Medicine 39, no. 02 (March 26, 2018): 181–98. http://dx.doi.org/10.1055/s-0037-1617424.

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AbstractDespite significant progress in the field of transplant immunology, acute cellular rejection (ACR) remains a very frequent complication after lung transplantation (LTx), with almost 30% of LTx recipients experiencing at least one episode of treated ACR during the first year of follow-up. Most episodes respond to the first-line immunosuppressive treatment and are rarely a direct cause of death. However, the association of ACR with later adverse outcomes, such as chronic lung allograft dysfunction, bronchial stricture, and infectious complications associated with the intensification of immunosuppression, negatively impacts long-term survival. The burden imposed on patients and health-care resources is even higher in cases of refractory or recurrent ACR, which accelerates lung function decline. Although important laboratory and clinical research conducted over the last two decades has improved our understanding of the mechanisms underlying ACR, there are still many uncertainties about the risk factors for ACR, the optimal monitoring strategies, and the prediction of long-term outcomes. These knowledge gaps contribute to the large variability in clinical practice among LTx centers, which renders multicenter studies of ACR challenging. In this review, we summarize current evidence on the epidemiology, pathogenesis, and risk factors of ACR. We describe diagnostic and therapeutic approaches that are currently used in the clinical practice and also review promising diagnostic tools that are under investigation. Associations between ACR and other adverse outcomes of LTx are examined. Finally, within each topic of discussion, we highlight the main areas of controversy and opportunities for future research.

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25

Vega, A., D. Garcı́a-Alonso, A. Ramos, J. C. Ruiz, J. Castillo, M. G. Fleitas, M. Arias, and G. Pino-Chavez. "Immunohistochemical study of experimental acute cellular rejection." Transplantation Proceedings 34, no. 2 (March 2002): 731–32. http://dx.doi.org/10.1016/s0041-1345(02)02628-3.

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26

ROSENBERG, AMY S., TOSHIAKI MIZUOCHI, and ALFRED SINGER. "Cellular Interactions Resulting in Skin-Allograft Rejection." Annals of the New York Academy of Sciences 532, no. 1 Cytotoxic T C (August 1988): 76–85. http://dx.doi.org/10.1111/j.1749-6632.1988.tb36328.x.

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27

Colvin, R. B. "Cellular and Molecular Mechanisms of Allograft Rejection." Annual Review of Medicine 41, no. 1 (February 1990): 361–75. http://dx.doi.org/10.1146/annurev.me.41.020190.002045.

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28

Merten, Steven, Ju Chuan Chen, Hong Ha, Karren Plain, Rochelle A. Boyd, Mark J. Penny, Peter Leenaerts, and Bruce M. Hall. "THE CELLULAR BASIS OF CARDIAC ALLOGRAFT REJECTION." Transplantation 65, no. 9 (May 1998): 1152–58. http://dx.doi.org/10.1097/00007890-199805150-00002.

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29

Kulkarni, Anand V., Shiv K. Sarin, Ashok Choudhury, S. M. Shashthry, Karan Kumar, and Lovkesh Anand. "Role of microRNA in acute cellular rejection." Hepatology 65, no. 4 (February 21, 2017): 1423–24. http://dx.doi.org/10.1002/hep.29063.

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30

McManigle, William, Elizabeth Pavlisko, and Tereza Martinu. "Acute Cellular and Antibody-Mediated Allograft Rejection." Seminars in Respiratory and Critical Care Medicine 34, no. 03 (July 2, 2013): 320–35. http://dx.doi.org/10.1055/s-0033-1348471.

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31

DʼANTIGA, LORENZO, ANIL DHAWAN, BERNARD PORTMANN, RUGGIERO FRANCAVILLA, MOHAMMED RELA, NIGEL HEATON, and GIORGINA MIELI-VERGANI. "LATE CELLULAR REJECTION IN PAEDIATRIC LIVER TRANSPLANTATION." Transplantation 73, no. 1 (January 2002): 80–84. http://dx.doi.org/10.1097/00007890-200201150-00015.

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32

MARTIN, SUSAN, COLIN D. SHORT, WILLIAM LAWLER, RAMANLAL GOKAL, ROBERT W. G. JOHNSON, and NETAR P. MALLICK. "LATE CELLULAR REJECTION IN RENAL TRANSPLANT RECIPIENTS." Transplantation 41, no. 2 (February 1986): 262–63. http://dx.doi.org/10.1097/00007890-198602000-00025.

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33

Martinu, Tereza, Elizabeth N. Pavlisko, Dong-Feng Chen, and Scott M. Palmer. "Acute Allograft Rejection: Cellular and Humoral Processes." Clinics in Chest Medicine 32, no. 2 (June 2011): 295–310. http://dx.doi.org/10.1016/j.ccm.2011.02.008.

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34

van Agteren, Madelon, Willem Weimar, Annelies E. de Weerd, Peter A. W. te Boekhorst, Jan N. M. Ijzermans, Jaqueline van de Wetering, and Michiel G. H. Betjes. "The First Fifty ABO Blood Group Incompatible Kidney Transplantations: The Rotterdam Experience." Journal of Transplantation 2014 (2014): 1–6. http://dx.doi.org/10.1155/2014/913902.

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This study describes the single center experience and long-term results of ABOi kidney transplantation using a pretransplantation protocol involving immunoadsorption combined with rituximab, intravenous immunoglobulins, and triple immune suppression. Fifty patients received an ABOi kidney transplant in the period from 2006 to 2012 with a follow-up of at least one year. Eleven antibody mediated rejections were noted of which 5 were mixed antibody and cellular mediated rejections. Nine cellular mediated rejections were recorded. Two grafts were lost due to rejection in the first year. One-year graft survival of the ABOi grafts was comparable to 100 matched ABO compatible renal grafts, 96% versus 99%. At 5-year follow-up, the graft survival was 90% in the ABOi versus 97% in the control group. Posttransplantation immunoadsorption was not an essential part of the protocol and no association was found between antibody titers and subsequent graft rejection. Steroids could be withdrawn safely 3 months after transplantation. Adverse events specifically related to the ABOi protocol were not observed. The currently used ABOi protocol shows good short and midterm results despite a high rate of antibody mediated rejections in the first years after the start of the program.

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35

Hatoum, Hilana H., Anita Patel, and K. K. Venkat. "The Utility of Serial Allograft Biopsies during Delayed Graft Function in Renal Transplantation under Current Immunosuppressive Regimens." ISRN Nephrology 2014 (March 5, 2014): 1–3. http://dx.doi.org/10.1155/2014/292305.

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Delayed graft function (DGF) of kidney transplants increases risk of rejection. We aimed to assess the utility of weekly biopsies during DGF in the setting of currently used immunosuppression and identify variables associated with rejection during DGF. We reviewed all kidney transplants at our institution between January 2008 and December 2011. All patients received rabbit antithymocyte globulin/Thymoglobulin (ATG) or Basiliximab/Simulect induction with maintenance tacrolimus + mycophenolate + corticosteroid therapy. Patients undergoing at least one weekly biopsy during DGF comprised the study group. Eighty-three/420 (19.8%) recipients during this period experienced DGF lasting ≥1 week and underwent weekly biopsies until DGF resolved. Biopsy revealed significant rejection only in 4/83 patients (4.8%) (one Banff 1-A and two Banff 2-A cellular rejections, and one acute humoral rejection). Six other/83 patients (7.2%) had Banff-borderline rejection of uncertain clinical significance. Four variables (ATG versus Basiliximab induction, patient age, panel reactive anti-HLA antibody level at transplantation, and living versus deceased donor transplants) were statistically significantly different between patients with and without rejection, though the clinical significance of these differences is questionable given the low incidence of rejection. Conclusions. Under current immunosuppression regimens, rejection during DGF is uncommon and the utility of serial biopsies during DGF is limited.

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36

Mubarak, M. "Plasma cell-rich acute rejection: A morphologic archetype of combined cellular and humoral rejectione?" Indian Journal of Nephrology 26, no. 3 (2016): 157. http://dx.doi.org/10.4103/0971-4065.161520.

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37

Liu, Hong, Dolly Tyan, and Ge Chen. "P056 Cellular crossmatch (CXM) by flowspot predicts cellular rejection in kidney transplantation." Human Immunology 78 (September 2017): 95. http://dx.doi.org/10.1016/j.humimm.2017.06.116.

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38

Coelho, Fabricio Ferreira, Rafael Ferreira Coelho, Paulo Celso Bosco Massarollo, and Sérgio Mies. "Use of tacrolimus in rescue therapy of acute and chronic rejection in liver transplantation." Revista do Hospital das Clínicas 58, no. 3 (2003): 141–46. http://dx.doi.org/10.1590/s0041-87812003000300003.

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PURPOSE: To study the indications and results of tacrolimus as rescue therapy for acute cellular or chronic rejection in liver transplantation. PATIENTS AND METHODS: Eighteen liver transplant recipients who underwent rescue therapy with tacrolimus between March 1995 and August 1999 were retrospectively studied. The treatment indication, patients, and graft situation were recorded as of October 31st, 1999. The response to tacrolimus was defined as patient survival with a functional graft and histological reversal of acute cellular, or for chronic rejection, bilirubin serum levels decreasing to up to twice the upper normal limit. RESULTS: Fourteen cases (77.8%) presented a good response. The response rate for the different indications was: (1) acute cellular + sepsis - 0/1 case; (2) recurrent acute cellular - 1/1 case; (3) OKT3-resistant acute cellular - 2/2 cases; (4) steroid-resistant acute cellular + active viral infection - 3/3 cases; (5) chronic rejection - 8/11 cases (72.7% response rate). The 4 patients who did not respond died. CONCLUSION: Tacrolimus rescue therapy was successful in most cases of acute cellular and chronic rejection in liver transplantation.

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39

Fozouni, Laila, Adrienne Lebsack, Yara Mohamad, Chris Freise, Peter Stock, and Jennifer Lai. "3485 Frailty Associated with Increased Rates of Acute Cellular Rejection Within 3 Months After Liver Transplantation." Journal of Clinical and Translational Science 3, s1 (March 2019): 144. http://dx.doi.org/10.1017/cts.2019.328.

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OBJECTIVES/SPECIFIC AIMS: There is currently a gap in the literature regarding the relationship between acute cellular rejection and frailty in LT patients. We aimed to evaluate the association between frailty and acute cellular rejection in LT patients. METHODS/STUDY POPULATION: Included were LT recipients from 2014-16 at a single center who had a frailty assessment prior to LT using the Liver Frailty index consisting of grip strength, chair stands, and balance. Frailty was defined by a Liver Frailty Index > 4.5. Data on acute cellular rejection at 3 months (primary outcome) and immunosuppression regimens were collected from medical chart review. Univariable and multivariable logistic regression assessed the associations between frailty and acute cellular rejection. RESULTS/ANTICIPATED RESULTS: A total of 241 LT recipients were included. Of these, 37% were female, 55% had Hepatitis C, and the median (IQR) age was 60 (54-65); 46 (19%) were classified as frail. 98% of patients were on a combination of mycophenolate, corticosteroids and tacrolimus on discharge compared to 80% by 3 months. Within the first 3 months post-LT, 7 (15%) of frail patients versus 10 (5%) (p = 0.02) of non-frail patients experienced acute cellular rejection. In univariable logistic regression, frailty was associated with a 3.3 times higher odds of acute cellular rejection at 3 months (95%CI 1.19, 9.26, p = 0.02); age (OR 0.91), Black race (OR 3.2), autoimmune disease (OR 2.3), and diabetes (OR 0.3) were also associated with acute cellular rejection at 3 months with a p-value<0.20. In a multivariate analysis, after adjusting for age, frailty remained significantly associated with rejection (OR 3.06, 95%CI 1.04, 9.01, p = 0.043). There were no significant differences in immunosuppression regimens or rates of mycophenolate dose reduction in the first 3 months between frail and non-frail patients. DISCUSSION/SIGNIFICANCE OF IMPACT: Frailty is associated with an increased rate of acute cellular rejection within 3 months post-LT, despite similar immunosuppression regimens and doses. Future studies should evaluate whether frailty should be considered in the management of immunosuppression in the early post-transplant period.

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40

Bedáňová, Helena, Jan Černý, Erik Petrikovits, Pavel Studeník, Olga Janíčková, Jiří Ondrášek, Petr Němec, Lenka Špinarová, and Alžběta Sirotková. "Heart retransplantation for undiagnosed severe acute cellular rejection." Cor et Vasa 50, no. 10 (October 1, 2008): 396–98. http://dx.doi.org/10.33678/cor.2008.139.

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41

Pino-Chavez, Gilda. "Differentiating Acute Humoral from Acute Cellular Rejection Histopathologically." Graft 4, no. 1 (January 2001): 60–62. http://dx.doi.org/10.1177/152216280100400116.

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El Gamel, A., S. Grant, N. Yonan, B. Keevil, T. Aziz, A. K. Deiraniya, C. Campbell, A. Rahman, P. Haselton, and I. V. Hutchinson. "Interleukin-10 and cellular rejection following cardiac transplantation." Transplantation Proceedings 30, no. 5 (August 1998): 2387–88. http://dx.doi.org/10.1016/s0041-1345(98)00663-0.

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Jkw, Wong, Lehnert A, Davey K, Hawthorne W, and O'Connell PJ. "CHEMOKINES ARE IMPORTANT INITIATORS OF CELLULAR XENOGRAFT REJECTION." Nephrology 7, no. 1 (February 2002): A115. http://dx.doi.org/10.1046/j.1440-1797.2002.00007-1-115.x.

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Dengler, T. "Cellular and molecular biology of cardiac transplant rejection." Journal of Nuclear Cardiology 7, no. 6 (November 2000): 669–85. http://dx.doi.org/10.1067/mnc.2000.111128.

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Yamamoto, Naoki, Kuniko Einaga-Naito, Manabu Kuriyama, Yukimichi Kawada, and Ryotaro Yoshida. "CELLULAR BASIS OF SKIN ALLOGRAFT REJECTION IN MICE." Transplantation 65, no. 6 (March 1998): 818–25. http://dx.doi.org/10.1097/00007890-199803270-00009.

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Greer, Mark, Christopher Werlein, and Danny Jonigk. "Surveillance for acute cellular rejection after lung transplantation." Annals of Translational Medicine 8, no. 6 (March 2020): 410. http://dx.doi.org/10.21037/atm.2020.02.127.

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Gupta, Siddhartha Datta, Mark Hudson, Andrew K. Burroughs, Richard Morris, Keith Rolles, Peter Amlot, Peter J. Scheuer, and Amar P. Dhillon. "Grading of cellular rejection after orthotopic liver transplantation." Hepatology 21, no. 1 (January 1995): 46–57. http://dx.doi.org/10.1002/hep.1840210110.

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Nagral, Aabha, Ziv Ben-Ari, Amar Paul Dhillon, and Andrew Kenneth Burroughs. "Eosinophils in acute cellular rejection in liver allografts." Liver Transplantation and Surgery 4, no. 5 (September 1998): 355–62. http://dx.doi.org/10.1002/lt.500040503.

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Ashokkumar, Chethan, Kyle Soltys, George Mazariegos, Geoffrey Bond, Brandon W. Higgs, Mylarappa Ningappa, Qing Sun, et al. "Predicting Cellular Rejection With a Cell-Based Assay." Transplantation 101, no. 1 (January 2017): 131–40. http://dx.doi.org/10.1097/tp.0000000000001076.

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Yoshizawa, S., O. Nikolskaia, L. A. Batoroeva, Y. K. Batoroev, O. Leone, C. Toquet, J. Duong Van Huyen, et al. "An International Tutorial for Cardiac Acute Cellular Rejection." Journal of Heart and Lung Transplantation 33, no. 4 (April 2014): S314—S315. http://dx.doi.org/10.1016/j.healun.2014.01.851.

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