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Journal articles on the topic 'Immunosuppression'

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Author: Grafiati

Published: 4 June 2021

Last updated: 30 July 2024

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1

Eisner, F., M. Küper, F. Ziegler, D. Zieker, A. Königsrainer, and J. Glatzle. "Impact of Perioperative Immunosuppressive Medication on Surgical Outcome in Crohn’s Disease (CD)." Zeitschrift für Gastroenterologie 52, no. 05 (May 2014): 436–40. http://dx.doi.org/10.1055/s-0033-1356347.

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Abstract Introduction: Patients with Crohn’s disease [CD] carry an 80 − 90 % lifetime risk of undergoing surgery. Many of these patients are on immunosuppressive medication at the time of surgery. The aim of this study was to evaluate the effect of immunosuppression on the surgical outcome in CD patients. Methods: We retrospectively analyzed 484 consecutive abdominal operations for CD from 1995 to 2008 for surgical complications. Results: A total of 241 operations (= 49.8 %) were performed under perioperative immunosuppression (corticoids and thiopurine). The overall complication rate was 18.6 %, the major complication rate was 8.7 % and the anastomotic leakage rate was 3.3 %. No differences were observed between patients without immunosuppression compared to those with immunosuppression. Patients with colo-rectal resections showed a higher complication rate than patients with small bowel resection independently of immunosuppression. Conclusion: Nearly 50 % of the patients undergoing abdominal surgery for CD are receiving immunosuppressive medication during surgery. However, perioperative immunosuppression with corticoids, thiopurine or the combination of both does not significantly alter the surgical complication rate. Therefore the decision of a required surgery should not be delayed due to the fact that the patient is under immunosuppressive medication.

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2

Ngobili, Terrika A., and Michael A. Daniele. "Nanoparticles and direct immunosuppression." Experimental Biology and Medicine 241, no. 10 (May 2016): 1064–73. http://dx.doi.org/10.1177/1535370216650053.

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Targeting the immune system with nanomaterials is an intensely active area of research. Specifically, the capability to induce immunosuppression is a promising complement for drug delivery and regenerative medicine therapies. Many novel strategies for immunosuppression rely on nanoparticles as delivery vehicles for small-molecule immunosuppressive compounds. As a consequence, efforts in understanding the mechanisms in which nanoparticles directly interact with the immune system have been overshadowed. The immunological activity of nanoparticles is dependent on the physiochemical properties of the nanoparticles and its subsequent cellular internalization. As the underlying factors for these reactions are elucidated, more nanoparticles may be engineered and evaluated for inducing immunosuppression and complementing immunosuppressive drugs. This review will briefly summarize the state-of-the-art and developments in understanding how nanoparticles induce immunosuppressive responses, compare the inherent properties of nanomaterials which induce these immunological reactions, and comment on the potential for using nanomaterials to modulate and control the immune system.

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3

Schuurmans, Macé M., Miro E. Raeber, Maurice Roeder, and René Hage. "Adaptive Immunosuppression in Lung Transplant Recipients Applying Complementary Biomarkers: The Zurich Protocol." Medicina 59, no. 3 (March 2, 2023): 488. http://dx.doi.org/10.3390/medicina59030488.

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Achieving adequate immunosuppression for lung transplant recipients in the first year after lung transplantation is a key challenge. Prophylaxis of allograft rejection must be balanced with the adverse events associated with immunosuppressive drugs, for example infection, renal failure, and diabetes. A triple immunosuppressive combination is standard, including a steroid, a calcineurin inhibitor, and an antiproliferative compound beginning with the highest levels of immunosuppression and a subsequent tapering of the dose, usually guided by therapeutic drug monitoring and considering clinical results, bronchoscopy sampling results, and additional biomarkers such as serum viral replication or donor-specific antibodies. Balancing the net immunosuppression level required to prevent rejection without overly increasing the risk of infection and other complications during the tapering phase is not well standardized and requires repeated assessments for dose-adjustments. In our adaptive immunosuppression approach, we additionally consider results from the white blood cell counts, in particular lymphocytes and eosinophils, as biomarkers for monitoring the level of immunosuppression and additionally use them as therapeutic targets to fine-tune the immunosuppressive strategy over time. The concept and its rationale are outlined, and areas of future research mentioned.

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4

Goldraich, Livia A., Santiago A. Tobar Leitão, Fernando L. Scolari, Fabiana G. Marcondes-Braga, Marcely G. Bonatto, Dipika Munyal, Jennifer Harrison, et al. "A Comprehensive and Contemporary Review on Immunosuppression Therapy for Heart Transplantation." Current Pharmaceutical Design 26, no. 28 (August 31, 2020): 3351–84. http://dx.doi.org/10.2174/1381612826666200603130232.

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: Heart transplantation is the standard of therapy for patients with end-stage heart disease. Since the first human-to-human heart transplantation, performed in 1967, advances in organ donation, surgical techniques, organ preservation, perioperative care, immunologic risk assessment, immunosuppression agents, monitoring of graft function and surveillance of long-term complications have drastically increased recipient survival. However, there are yet many challenges in the modern era of heart transplantation in which immunosuppression may play a key role in further advances in the field. A fine-tuning of immune modulation to prevent graft rejection while avoiding side effects from over immunosuppression has been the vital goal of basic and clinical research. Individualization of drug choices and strategies, taking into account the recipient's clinical characteristics, underlying heart failure diagnosis, immunologic risk and comorbidities seem to be the ideal approaches to improve post-transplant morbidity and survival while preventing both rejection and complications of immunosuppression. : The aim of the present review is to provide a practical, comprehensive overview of contemporary immunosuppression in heart transplantation. Clinical evidence for immunosuppressive drugs is reviewed and practical approaches are provided. Cardiac allograft rejection classification and up-to-date management are summarized. Expanding therapies, such as photophoresis, are outlined. Drug-to-drug interactions of immunosuppressive agents focused on cardiovascular medications are summarized. Special situations involving heart transplantation such as sarcoidosis, Chagas diseases and pediatric immunosuppression are also reviewed. The evolution of phamacogenomics to individualize immunosuppressive therapy is described. Finally, future perspectives in the field of immunosuppression in heart transplantation are highlighted.

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5

Spinner, Joseph A., and Susan W. Denfield. "Immunosuppressant Drugs and Their Effects on Children Undergoing Solid Organ Transplant." Pediatrics In Review 43, no. 2 (January 28, 2022): 71–86. http://dx.doi.org/10.1542/pir.2020-000620.

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More than 112,000 men, women, and children are awaiting solid organ transplant (SOT) as of March 2020, and more than 39,000 transplants were performed in the United States in 2019. Approximately 2,000 children undergo SOT every year in the United States, and the number of children awaiting SOT continues to increase. Immunosuppression is the mainstay of prevention and treatment of solid organ rejection, a significant source of morbidity and mortality after SOT. There are several different classes of immunosuppressive drugs, and the phases of immunosuppression after SOT can be divided into early, maintenance, and rescue therapies. The specific class and dose of drug will be determined by the type of organ transplant, time since transplant, phase of therapy, and other patient-specific considerations. The goal of the transplant team is to find the optimal balance between too little immunosuppression and too much immunosuppression. Too little immunosuppression can result in organ rejection, but too much immunosuppression can result in increased infections, increased malignancy, and adverse drug events such as nephrotoxicity. Although the specific drug choice and dosage will be managed by specialized transplant physicians, these immunosuppressive drugs have many drug interactions with commonly prescribed medications and require dose titration. To provide the best care to children who have received a SOT, pediatricians should be aware of these interactions and be able to distinguish routine pediatric concerns from transplant immunosuppression-related infections or complications. Current vaccine recommendations for children receiving immunosuppression after SOT are also discussed.

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6

Liu, Yuan-Yuan, Chang-Ping Li, Ming-Sheng Huai, Xiao-Meng Fu, Zhuang Cui, Lin-Lin Fan, Shu Zhang, et al. "Comprehensive Comparison of Three Different Immunosuppressive Regimens for Liver Transplant Patients with Hepatocellular Carcinoma: Steroid-Free Immunosuppression, Induction Immunosuppression and Standard Immunosuppression." PLOS ONE 10, no. 3 (March 27, 2015): e0120939. http://dx.doi.org/10.1371/journal.pone.0120939.

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7

Tsalouchos, Aris, and Maurizio Salvadori. "La terapia immunosoppressiva nel trapianto di rene." Giornale di Tecniche Nefrologiche e Dialitiche 31, no. 3 (September 2019): 192–96. http://dx.doi.org/10.1177/0394936219875392.

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Immunosuppressive therapy in renal transplantation Immunosuppressive therapy in renal transplantation can be distinguished in induction therapy and maintenance therapy. Induction therapy is an intense immunosuppressive therapy administered at the time of kidney transplantation to reduce the risk of acute allograft rejection. In general, the induction immunosuppressive strategies used at kidney transplant centers fall into one of these two categories. One strategy relies upon high doses of conventional immunosuppressive agents, while the other utilizes antibodies directed against T-cell antigens in combination with lower doses of conventional agents. Maintenance immunosuppressive therapy is administered to almost all kidney transplant recipients to help prevent acute rejection and loss of the renal allograft. Although an adequate level of immunosuppression is required to dampen the immune response to the allograft, the level of chronic immunosuppression is decreased over time (as the risk of acute rejection decreases) to help lower the overall risk of infection and malignancy; these risks directly correlate with the degree of overall immunosuppression. The optimal maintenance immunosuppressive therapy in kidney transplantation is not established. The major immunosuppressive agents that are available in various combination regimens are glucocorticoids (primarily oral prednisone), azathioprine, mycophenolate mofetil (MMF), enteric-coated mycophenolate sodium (EC-MPS), cyclosporine (in non-modified or modified [microemulsion] form), Tacrolimus, everolimus, rapamycin (sirolimus), and Belatacept.

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8

Himes, Benjamin, Cori Fain, Zachariah Tritz, Helen Li, Philipp Geiger, Timothy Peterson, and Ian Parney. "IMMU-15. HEPARIN INHIBITS THE EXTRACELLULAR VESICLE-MEDIATED INDUCTION OF IMMUNOSUPPRESSIVE MONOCYTES IN GLIOBLASTOMA." Neuro-Oncology 22, Supplement_2 (November 2020): ii107. http://dx.doi.org/10.1093/neuonc/noaa215.445.

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Abstract Glioblastoma (GBM) is the most common and fatal primary brain tumor in adults. The development of novel therapies is critical, as little has changed regarding the standard of care in nearly two decades. Immunotherapy holds much promise, as treatments including chimeric antigen receptor (CAR) T cells and immune checkpoint blockade inhibitors have transformed the treatment of a number of cancers in recent years. However, GBM patients exhibit profound immunosuppression, limiting the efficacy of these therapies. Understanding the mechanisms of GBM-mediated immunosuppression is critical to overcoming this barrier. GBM-derived extracellular vesicles (EVs) have been shown to mediate the induction of immunosuppressive monocytes, which may point to a mechanism of immunosuppression. EVs make initial contact with target cells through interactions between heparan sulfate proteoglycans, and soluble heparin has been shown to inhibit these interactions in some models. We demonstrate that soluble heparin inhibits the binding of GBM-derived EVs to monocytes in a dose-dependent manner, and that heparin treatment reduces the induction of immunosuppressive monocytes upon in vitro conditioning of monocytes with GBM-derived EVs (p< 0.01). Further, we demonstrate that heparin treated EV-conditioned monocytes are functionally less immunosuppressive than untreated EV-conditioned monocytes as measured by T cell proliferation in co-culture studies (p< 0.05). Taken together, these findings underscore the import of tumor-derived EVs in immunosuppression in GBM, and demonstrate the feasibility of targeting EV-monocyte interactions in treating GBM-mediated immunosuppression.

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9

Tsalouchos, Aris, and Maurizio Salvadori. "La terapia immunosoppressiva nel trapianto di rene." Giornale di Clinica Nefrologica e Dialisi 31, no. 3 (September 16, 2019): 192–96. http://dx.doi.org/10.33393/gcnd.2019.529.

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Immunosuppressive therapy in renal transplantation can be distinguished in induction therapy and maintenance therapy. Induction therapy is an intense immunosuppressive therapy administered at the time of kidney transplantation to reduce the risk of acute allograft rejection. In general, the induction immunosuppressive strategies used at kidney transplant centers fall into one of these two categories. One strategy relies upon high doses of conventional immunosuppressive agents, while the other utilizes antibodies directed against T-cell antigens in combination with lower doses of conventional agents. Maintenance immunosuppressive therapy is administered to almost all kidney transplant recipients to help prevent acute rejection and loss of the renal allograft. Although an adequate level of immunosuppression is required to dampen the immune response to the allograft, the level of chronic immunosuppression is decreased over time (as the risk of acute rejection decreases) to help lower the overall risk of infection and malignancy; these risks directly correlate with the degree of overall immunosuppression. The optimal maintenance immunosuppressive therapy in kidney transplantation is not established. The major immunosuppressive agents that are available in various combination regimens are glucocorticoids (primarily oral prednisone), azathioprine, mycophenolate mofetil (MMF), enteric-coated mycophenolate sodium (EC-MPS), cyclosporine (in non-modified or modified [microemulsion] form), Tacrolimus, everolimus, rapamycin (sirolimus), and Belatacept.

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10

Vella, John P., and Alexander C. Wiseman. "Immunosuppression." Nephrology Self-Assessment Program 18, no. 5 (November 2019): 285–92. http://dx.doi.org/10.1681/nsap.2019.18.5.6.

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11

Derek, Elika, and Kiran Dhanireddy. "Immunosuppression." Current Opinion in Organ Transplantation 17, no. 6 (December 2012): 616–18. http://dx.doi.org/10.1097/mot.0b013e32835a7d3a.

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12

Townend, Mike. "Immunosuppression." Practice Nursing 13, no. 8 (August 2002): 357–60. http://dx.doi.org/10.12968/pnur.2002.13.8.10804.

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13

Land, Walter. "Immunosuppression." Current Opinion in Organ Transplantation 5, no. 3 (September 2000): 243–44. http://dx.doi.org/10.1097/00075200-200009000-00013.

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14

Sher, Linda S. "Immunosuppression." Current Opinion in Organ Transplantation 6, no. 4 (December 2001): 311–12. http://dx.doi.org/10.1097/00075200-200112000-00007.

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15

Mathias, Judith M. "Immunosuppression." AORN Journal 41, no. 4 (April 1985): 748–61. http://dx.doi.org/10.1016/s0001-2092(07)66298-x.

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16

Porrett, Paige M., Sohaib K. Hashmi, and Abraham Shaked. "Immunosuppression." Clinics in Liver Disease 18, no. 3 (August 2014): 687–716. http://dx.doi.org/10.1016/j.cld.2014.05.012.

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17

Kumar, Ram S., Christian G. Peyre, and Linda S. Sher. "Immunosuppression." Seminars in Anesthesia, Perioperative Medicine and Pain 23, no. 1 (March 2004): 12–22. http://dx.doi.org/10.1053/j.sane.2003.12.010.

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18

Sigal, Nolan H., and Matthew J. Wyvratt. "Immunosuppression." Perspectives in Drug Discovery and Design 2, no. 1 (August 1994): 1–2. http://dx.doi.org/10.1007/bf02171732.

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19

Yakubu, Idris, Abdolreza Haririan, Stephen Bartlett, and Tracy Sparkes. "Successful Renal Transplantation between Identical Twins with Very Brief Immunosuppression." Case Reports in Transplantation 2018 (June 27, 2018): 1–5. http://dx.doi.org/10.1155/2018/9842893.

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Renal transplantation between monozygous identical twins provides an opportunity to utilize minimal immunosuppression to maintain stable allograft function, thereby alleviating the toxicities of immunosuppressive therapy. Despite monozygosity, there is a possibility of discordant protein presentation in identical twins that could trigger alloimmune response and lead to graft injury. Therefore, the optimal immunosuppression regimen in this patient population is unknown, and the safety of immunosuppression withdrawal remains controversial. Herein, we describe two patients who underwent successful renal transplantation from monozygotic identical twin donors. Monozygosity was determined using short tandem repeat (STR) analysis. All immunosuppression was successfully discontinued at 2 days and 3 weeks, respectively, after transplantation. Both patients are alive with functioning renal grafts at 1 year and 5 years after transplant, respectively. These two cases suggest that immunosuppression can be withdrawn safely and rapidly in select monozygous identical twin renal transplant recipients.

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20

Li, Chi-Cheng, Rina Munalisa, Hsuan-Yun Lee, Te-Sheng Lien, Hao Chan, Shih-Che Hung, Der-Shan Sun, Ching-Feng Cheng, and Hsin-Hou Chang. "Restraint Stress-Induced Immunosuppression Is Associated with Concurrent Macrophage Pyroptosis Cell Death in Mice." International Journal of Molecular Sciences 24, no. 16 (August 17, 2023): 12877. http://dx.doi.org/10.3390/ijms241612877.

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Psychological stress is widely acknowledged as a major contributor to immunosuppression, rendering individuals more susceptible to various diseases. The complex interplay between the nervous, endocrine, and immune systems underlies stress-induced immunosuppression. However, the underlying mechanisms of psychological-stress-induced immunosuppression remain unclear. In this study, we utilized a restraint stress mouse model known for its suitability in investigating physiological regulations during psychological stress. Comparing it with cold exposure, we observed markedly elevated levels of stress hormones corticosterone and cortisol in the plasma of mice subjected to restraint stress. Furthermore, restraint-stress-induced immunosuppression differed from the intravenous immunoglobulin-like immunosuppression observed in cold exposure, with restraint stress leading to increased macrophage cell death in the spleen. Suppression of pyroptosis through treatments of inflammasome inhibitors markedly ameliorated restraint-stress-induced spleen infiltration and pyroptosis cell death of macrophages in mice. These findings suggest that the macrophage pyroptosis associated with restraint stress may contribute to its immunosuppressive effects. These insights have implications for the development of treatments targeting stress-induced immunosuppression, emphasizing the need for further investigation into the underlying mechanisms.

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21

Xie, Di, Hao Zhao, Xin Xu, Zhanmei Zhou, Cailing Su, Nan Jia, Youhua Liu, and Fan Fan Hou. "Intensity of Macrophage Infiltration in Glomeruli Predicts Response to Immunosuppressive Therapy in Patients with IgA Nephropathy." Journal of the American Society of Nephrology 32, no. 12 (October 20, 2021): 3187–96. http://dx.doi.org/10.1681/asn.2021060815.

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BackgroundThe lack of a tool for predicting the response to immunosuppressive therapy in IgA nephropathy (IgAN) limits patient-specific risk stratification and early treatment decision making. Models for predicting response to immunosuppression in IgAN that can be applied at the time of kidney biopsy are needed.MethodsThis prospective cohort study involved 621 Chinese patients with IgAN who were at high risk for disease progression and had persistent proteinuria ≥1 g/d, despite 3 months of optimized supportive care with renin-angiotensin system inhibitors. Participants received immunosuppressive therapy for a median of 18 months. We used immunochemistry to identify macrophage and lymphocyte infiltrates in biopsy specimens and digital image analysis to quantify them. The outcome was response to immunosuppression, defined as complete or partial remission within 12 months of immunosuppression.ResultsKidney infiltration of CD68+ and CD206+ macrophages increased in patients with IgAN. Having higher levels of glomerular CD206+ macrophage infiltration was associated with a 40-fold increased probability of response to immunosuppression in adjusted analysis compared with having lower levels. Patients with a higher intensity of glomerular CD68+ infiltrates had a 13-fold increase in probability of responding to immunosuppression. Intensity of glomerular CD206+ and CD68+ macrophage infiltration predicted the response to immunosuppression (area under the curve [AUC], 0.84; 95% CI, 0.81 to 0.88). The AUC increased to 0.87 (95% CI, 0.84 to 0.91) in a model combining the infiltration score of CD206+ and CD68+ infiltrates with the MEST-C score and clinical data at biopsy.ConclusionsIntensity of glomerular macrophage infiltration predicted response to immunosuppressive therapy in patients with IgAN who were at high risk of progression, and may help physicians identify patients who will benefit from such treatment.

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22

Cajanding, Ruff. "Immunosuppression following organ transplantation. Part 1: mechanisms and immunosuppressive agents." British Journal of Nursing 27, no. 16 (September 6, 2018): 920–27. http://dx.doi.org/10.12968/bjon.2018.27.16.920.

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23

Moertel, Christopher, Junzhe Xi, and Michael R. Olin. "Understanding and overcoming the immunosuppressive effects of glioma induced immunosuppression." Journal for ImmunoTherapy of Cancer 1, Suppl 1 (2013): P169. http://dx.doi.org/10.1186/2051-1426-1-s1-p169.

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24

Zou, Weiping, and Yatrik M. Shah. "A PHD in immunosuppression: oxygen-sensing pathways regulate immunosuppressive Tregs." Journal of Clinical Investigation 129, no. 9 (July 29, 2019): 3524–26. http://dx.doi.org/10.1172/jci130009.

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25

Dittmer, Ulf, Diane M. Brooks, and Kim J. Hasenkrug. "Protection against Establishment of Retroviral Persistence by Vaccination with a Live Attenuated Virus." Journal of Virology 73, no. 5 (May 1, 1999): 3753–57. http://dx.doi.org/10.1128/jvi.73.5.3753-3757.1999.

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ABSTRACT Many human viruses not only cause acute diseases but also establish persistent infections. Such persistent viruses can cause chronic diseases or can reactivate to cause acute diseases in AIDS patients or patients receiving immunosuppressive therapies. While the prevention of persistent infections is an important consideration in the design of modern vaccines, surprisingly little is known about this aspect of protection. In the current study, we tested the feasibility of vaccine prevention of retroviral persistence by using a Friend virus model that we recently developed. In this model, persistent virus can be detected at very low levels by immunosuppressing the host to reactivate virus or by transferring persistently infected spleen cells into highly susceptible mice. Two vaccines were analyzed, a recombinant vaccinia virus vector expressing Friend virus envelope protein and a live attenuated Friend virus. Both vaccines reduced pathogenic virus loads to levels undetectable by infectious center assays. However, only the live, attenuated vaccine prevented immunosuppression-induced reactivation of persistent virus. Thus, even very low levels of persistent Friend virus posed a significant threat during immunosuppression. Our results demonstrate that vaccine protection against establishment of retroviral persistence is attainable.

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Ayasoufi, Katayoun, Zachariah Tritz, Cori Fain, Roman Khadka, Fang Jin, Michael Hansen, and Aaron Johnson. "IMMU-19. EVALUATING EFFECTS OF REVERSING DISTINCT FACETS OF IMMUNOSUPPRESSION IN EXPERIMENTAL GBM." Neuro-Oncology 23, Supplement_6 (November 2, 2021): vi95—vi96. http://dx.doi.org/10.1093/neuonc/noab196.378.

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Abstract Glioblastoma is associated with severe and multifaceted immunosuppression affecting all immune organs. Immunosuppression in GBM is a critical barrier to the success of immunotherapies and patient survival. We demonstrated that immunosuppression in the GL261-model of experimental GBM presents with significant thymic and spleen atrophy, MHCII downregulation, presence of potent immunosuppressive factors in serum, and sequestration of T-cells in the bone marrow. Parabiosis studies determined that soluble factors mediate immunosuppression by inhibiting T-cell proliferation, thymic involution, and loss of peripheral T-cells. In contrast, bone marrow T-cell sequestration was not mediated through soluble factors. While the immunosuppression in GBM is severe, a causative link between each facet of immunosuppression and overall survival is lacking. We used two strategies to block T-cell sequestration into the bone marrow and evaluated the extent survival was impacted in experimental GBM. First, we evaluated the extent a novel and off-the-shelf combination immunotherapy that uses extended 1/2-life IL-2 and anti-PD-1 reverses bone marrow T-cell sequestration. Sham treatment or anti-PD1 monotherapy did not alter T-cell sequestration in the bone marrow and animals had no enhanced survival. Extended 1/2-life IL-2 monotherapy and combination strategy both prevented T-cell sequestration into the bone marrow. However, only combined therapy, which also prevented MHC class II downregulation, improved survival. Second, we determined that glioma-bearing adrenalectomized mice do not present with bone marrow T-cell sequestration. However, sera of glioma-bearing adrenalectomized mice is as immunosuppressive as glioma-bearing controls. Blocking bone marrow T-cell sequestration in the presences of serum immunosuppression led to no survival benefit in glioma-bearing adrenalectomized mice compared to controls. In short, bone marrow T-cell sequestration alone does not correspond with overall survival in experimental glioma. Importantly, a concerted effort to reverse MHC class II downregulation and define inhibitory circulating factors may have the highest impact in immunotherapeutic efficacy and improving patient survival.

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Guo, Richard F., Frew H. Gebreab, Emily Hsiang-Ho Tang, Zhe Piao, Steve S. Lee, and Mario L. Perez. "Cutaneous Ulcer as Leading Symptom of Systemic Cytomegalovirus Infection." Case Reports in Infectious Diseases 2015 (2015): 1–4. http://dx.doi.org/10.1155/2015/723962.

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Cytomegalovirus (CMV) infection rarely manifests with skin ulcerations. We describe a case report of a 64-year-old woman with chronic immunosuppression for treatment of mixed connective tissue disease, presenting with new onset leg ulcerations after a recent change in immunosuppressive regimen. She subsequently developed fulminant hepatitis, encephalopathy, and pancytopenia and was found to have severe systemic CMV viremia. Skin ulcer biopsy was positive by immunohistochemical staining for CMV infected endothelial cells. Both systemic disease and skin ulcer rapidly improved after stopping immunosuppression and administering intravenous ganciclovir. New onset skin ulcers in an immunosuppressed individual, especially with recent changes in immunosuppressive regimen, should raise the suspicion of reactivation of CMV.

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Wang, Hua, Miguel C. Sobral, Tracy Snyder, Yevgeny Brudno, Vijay S. Gorantla, and David J. Mooney. "Clickable, acid labile immunosuppressive prodrugs for in vivo targeting." Biomaterials Science 8, no. 1 (2020): 266–77. http://dx.doi.org/10.1039/c9bm01487j.

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Padovani, Cristina M., and Kingsley Yin. "Immunosuppression in Sepsis: Biomarkers and Specialized Pro-Resolving Mediators." Biomedicines 12, no. 1 (January 13, 2024): 175. http://dx.doi.org/10.3390/biomedicines12010175.

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Severe infection can lead to sepsis. In sepsis, the host mounts an inappropriately large inflammatory response in an attempt to clear the invading pathogen. This sustained high level of inflammation may cause tissue injury and organ failure. Later in sepsis, a paradoxical immunosuppression occurs, where the host is unable to clear the preexisting infection and is susceptible to secondary infections. A major issue with sepsis treatment is that it is difficult for physicians to ascertain which stage of sepsis the patient is in. Sepsis treatment will depend on the patient’s immune status across the spectrum of the disease, and these immune statuses are nearly polar opposites in the early and late stages of sepsis. Furthermore, there is no approved treatment that can resolve inflammation without contributing to immunosuppression within the host. Here, we review the major mechanisms of sepsis-induced immunosuppression and the biomarkers of the immunosuppressive phase of sepsis. We focused on reviewing three main mechanisms of immunosuppression in sepsis. These are lymphocyte apoptosis, monocyte/macrophage exhaustion, and increased migration of myeloid-derived suppressor cells (MDSCs). The biomarkers of septic immunosuppression that we discuss include increased MDSC production/migration and IL-10 levels, decreased lymphocyte counts and HLA-DR expression, and increased GPR18 expression. We also review the literature on the use of specialized pro-resolving mediators (SPMs) in different models of infection and/or sepsis, as these compounds have been reported to resolve inflammation without being immunosuppressive. To obtain the necessary information, we searched the PubMed database using the keywords sepsis, lymphocyte apoptosis, macrophage exhaustion, MDSCs, biomarkers, and SPMs.

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Barraclough, Katherine A., Nicole M. Isbel, Christine E. Staatz, and David W. Johnson. "BK Virus in Kidney Transplant Recipients: The Influence of Immunosuppression." Journal of Transplantation 2011 (2011): 1–9. http://dx.doi.org/10.1155/2011/750836.

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The incidence of BK virus infection in kidney transplant recipients has increased over recent decades, coincident with the use of more potent immunosuppression. More importantly, posttransplant BK virus replication has emerged as an important cause of graft damage and subsequent graft loss. Immunosuppression has been accepted as a major risk for BK virus replication. However, the specific contribution of individual immunosuppressive medications to this risk has not been well established. The purpose of this paper is to provide an overview of the recent literature on the influence of the various immunosuppressant drugs and drug combinations on posttransplant BK virus replication. Evidence supporting the various immunosuppression reduction strategies utilised in the management of BK virus will also be briefly discussed.

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Mickler, Thomas A., and David E. Longnecker. "The Immunosuppressive Aspects of Blood Transfusion." Journal of Intensive Care Medicine 7, no. 4 (July 1992): 176–88. http://dx.doi.org/10.1177/088506669200700405.

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Blood transfusion is associated with immunosuppression, although the exact etiology of the immunosuppressive effect is not fully understood. The clinical significance of the immunosuppressive effect of blood transfusion has been examined in three situations: (1) studies of renal allograft survival after renal transplantation, (2) outcome studies in patients who have had surgical resection of solid cancer tumors, and (3) studies of infection rates in postoperative patients. In each scenario, the data support the conclusion that transfusion is associated with immunosuppression as manifested by increased renal allograft survival, increased recurrence and mortality rates in patients with cancer, and increased infection rates in postoperative patients who are transfused. Not all studies demonstrate an immunosuppressive effect of transfusion. There are several possible explanations for these discrepancies. First, prognostic variables other than transfusion itself account for the outcome results in these retrospective studies. Second, the extent of immunosuppression may be influenced by the type of blood product transfused, the amount transfused, and the timing of the transfusion; these factors have not been considered in all studies. For example, whole blood has been implicated as having a greater immunosuppressive effect than packed red blood cells, and many studies have shown that more than three units of packed red blood cells are necessary to affect outcome. Controlled animal studies have tested the hypothesis that transfusions increase solid tumor growth or the risk for infection. These studies have yielded conflicting results. Nevertheless, evidence that blood transfusion influences clinical outcome mitigates that a decision to transfuse must consider both risks and benefits of a transfusion; the possible consequences of immunosuppression must be included among the risks. Use of autologous blood, erythropoietin, and, in the future, synthetic hemoglobin may lead to improved outcome in patients with certain disease processes.

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Ayasoufi, Katayoun, Christian K. Pfaller, Roman Khadka, Fang Jin, Jiaying Zheng, Matthew R. Schuelke, Laura Evgin, et al. "A generalized pathway of immunocompromise following central nervous system insult: the release of large immunosuppressive molecules and thymic involution." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 72.12. http://dx.doi.org/10.4049/jimmunol.204.supp.72.12.

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Abstract Immunosuppression following damage to the CNS is a common, yet poorly understood, feature of neurological diseases as diverse as stroke, traumatic brain injury, and glioblastoma. This immunosuppression is a barrier to successful patient outcomes. We sought to define the effect of various brain insults on the thymus and T-cell responses. We tested thymic function following various neurological insults, including viral infection, brain tumor, sterile inflammation, physical injury, and seizures. All brain insults resulted in significant thymic involution that was reversible if the insult was cleared. Thymic involution did not occur following similar peripheral insults. Using parabiosis, we demonstrated that thymic involution was transferable via circulatory routes from glioma-bearing to non-tumor-bearing parabionts. Similarly, serum obtained from mice with ongoing neurological insults potently inhibited T-cell proliferation in vitro. We next fractionated the serum based on molecular weight and tested the resulting fractions’ immunosuppressive potential. Interestingly, we found that serum fractions with large molecular weights of greater than 100 kiloDaltons were responsible for the immunosuppressive properties of serum obtained from glioma-bearing mice. In short, CNS-specific insults, regardless of nature, induce immunosuppression by prompting thymic involution and systemic immunosuppression mediated through circulating factors with large molecular weight. These studies provide evidence of the mechanisms leading to immune deficiencies observed in patients following neurological injuries.

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Ghosh, Mitrajit, Anna M. Lenkiewicz, and Bozena Kaminska. "The Interplay of Tumor Vessels and Immune Cells Affects Immunotherapy of Glioblastoma." Biomedicines 10, no. 9 (September 15, 2022): 2292. http://dx.doi.org/10.3390/biomedicines10092292.

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Immunotherapies with immune checkpoint inhibitors or adoptive cell transfer have become powerful tools to treat cancer. These treatments act via overcoming or alleviating tumor-induced immunosuppression, thereby enabling effective tumor clearance. Glioblastoma (GBM) represents the most aggressive, primary brain tumor that remains refractory to the benefits of immunotherapy. The immunosuppressive immune tumor microenvironment (TME), genetic and cellular heterogeneity, and disorganized vasculature hinder drug delivery and block effector immune cell trafficking and activation, consequently rendering immunotherapy ineffective. Within the TME, the mutual interactions between tumor, immune and endothelial cells result in the generation of positive feedback loops, which intensify immunosuppression and support tumor progression. We focus here on the role of aberrant tumor vasculature and how it can mediate hypoxia and immunosuppression. We discuss how immune cells use immunosuppressive signaling for tumor progression and contribute to the development of resistance to immunotherapy. Finally, we assess how a positive feedback loop between vascular normalization and immune cells, including myeloid cells, could be targeted by combinatorial therapies with immune checkpoint blockers and sensitize the tumor to immunotherapy.

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Scheinberg, Phillip, Steven H. Fischer, Li Li, Olga Nunez, Colin O. Wu, Elaine M. Sloand, Jeffrey I. Cohen, Neal S. Young, and A. John Barrett. "Distinct EBV and CMV reactivation patterns following antibody-based immunosuppressive regimens in patients with severe aplastic anemia." Blood 109, no. 8 (December 5, 2006): 3219–24. http://dx.doi.org/10.1182/blood-2006-09-045625.

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Abstract The natural history of EBV and CMV reactivation and the potential for serious complications following antibody-based immunosuppressive treatment for bone marrow failure syndromes in the absence of transplantation is not known. We monitored blood for EBV and CMV reactivation by polymerase chain reaction (PCR) weekly in 78 consecutive patients (total of 99 immunosuppressive courses) with aplastic anemia. Four regimens were studied: (1) HC, horse ATG/cyclosporine; (2) HCS, horse ATG/CsA/sirolimus; (3) RC, rabbit ATG/CsA; and (4) CP, alemtuzumab. There were no cases of EBV or CMV disease, but EBV reactivation occurred in 82 (87%) of 94 and CMV reactivation in 19 (33%) of 57 seropositive patients after starting immunosuppression. The median peak EBV copies were higher in the RC group when compared with HC, HCS, and alemtuzumab (P < .001). The median duration of PCR positivity for EBV was higher in the RC group compared with HC, HCS, and alemtuzumab (P = .001). Subclinical reactivation of both EBV and CMV is common and nearly always self-limited in patients with bone marrow failure receiving immunosuppression; different regimens are associated with different intensity of immunosuppression as measured by viral load and lymphocyte count; and viral reactivation patterns differ according to immunosuppressive regimens.

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Dittmer, Ulf, Brent Race, Karin E. Peterson, Ingunn M. Stromnes, Ronald J. Messer, and Kim J. Hasenkrug. "Essential Roles for CD8+ T Cells and Gamma Interferon in Protection of Mice against Retrovirus-Induced Immunosuppression." Journal of Virology 76, no. 1 (January 1, 2002): 450–54. http://dx.doi.org/10.1128/jvi.76.1.450-454.2002.

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ABSTRACT It is known that both animal and human retroviruses typically cause immunosuppression in their respective hosts, but the mechanisms by which this occurs are poorly understood. The present study uses Friend virus (FV) infections of mice as a model to determine how major histocompatibility complex (MHC) genes influence immunosuppression. Previously, MHC-I genes were shown to influence antibody responses to potent antigenic challenges given during acute FV infection. The mapping of an immune response to an MHC-I gene implicated CD8+ T cells in the mechanism, so we directly tested for their role by using in vivo CD8+ T-cell depletions. Mice resistant to FV-induced immunosuppression became susceptible when they were depleted of CD8+ T cells. Resistance also required gamma interferon (IFN-γ), as in vivo neutralization of IFN-γ converted mice from a resistant to susceptible phenotype. On the other hand, susceptibility to FV-induced immunosuppression was dependent on the immunosuppressive cytokine, interleukin-10 (IL-10), as antibody responses were restored in susceptible mice when IL-10 function was blocked in vivo. Thus, FV-induced immunosuppression of antibody responses involves complex mechanisms controlled at least in part by CD8+ T cells.

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Kummer, U., S. Thierfelder, G. Hoffmann-Fezer, and R. Schuh. "In vivo immunosuppression by pan-T cell antibodies relates to their isotype and to their C1q uptake." Journal of Immunology 138, no. 12 (June 15, 1987): 4069–74. http://dx.doi.org/10.4049/jimmunol.138.12.4069.

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Abstract There is considerable interest in the use of monoclonal anti-T cell antibodies for immunosuppression during organ transplantation. However, the in vitro cytotoxic titers of these monoclonal reagents do not correlate with their immunosuppressive potency when injected in vivo. A relationship nevertheless seems to exist between immunosuppression and the isotype of anti-mouse Thy-1 antibodies, because among several anti-Thy-1 antibodies of mouse and rat origin, the only two found to cause immunosuppression in vivo belonged to the rat IgG2b and mouse IgG2a isotype. We show here that a quantitative positive correlation exists between an antibody-induced humoral effector mechanism and immunosuppression. We measured the uptake of the C1q complement subunit by polyclonal rabbit and rat anti-thymocyte globulin and also seven monoclonal anti-Thy-1 antibodies in an immunohistochemical assay or a radioimmunoassay. Immunosuppression was studied in a murine graft-vs-host and skin allograft model. Our results suggest strongly that a stable association between the C1 protein and a potential binding antibody is an essential prerequisite of antibody-dependent cell inhibition in vivo that suppresses the immunoresponse against strongly incompatible transplantation antigens.

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Jefferson, J. Ashley. "Complications of Immunosuppression in Glomerular Disease." Clinical Journal of the American Society of Nephrology 13, no. 8 (July 24, 2018): 1264–75. http://dx.doi.org/10.2215/cjn.01920218.

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Most glomerular diseases are immunologically mediated disorders of the kidney and are common causes of ESKD. In addition to supportive therapy, a wide range of immunosuppressive agents are used in the management of patients with these conditions. Immunosuppression requires a careful balance of risk and benefits, and many of these agents have a narrow therapeutic window and require close monitoring. This review describes the side effects of immunosuppressive agents used in recent randomized, controlled trials of glomerular disease, and highlights some of the key adverse events that determine the choice and prescription of these medications.

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Schnepp, E., and D. Kaminski. "Chronic Immunosuppression." Pediatrics in Review 33, no. 10 (October 1, 2012): 481–82. http://dx.doi.org/10.1542/pir.33-10-481.

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Shmaefsky, Brian R. "Why Immunosuppression?" Science News 132, no. 23 (December 5, 1987): 355. http://dx.doi.org/10.2307/3971705.

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Schnepp, Erin, and Dorota Kaminski. "Chronic Immunosuppression." Pediatrics In Review 33, no. 10 (October 1, 2012): 481–82. http://dx.doi.org/10.1542/pir.33.10.481.

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Barshes, Neal, R. "Pharmacologic immunosuppression." Frontiers in Bioscience 9, no. 1-3 (2004): 411. http://dx.doi.org/10.2741/1249.

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Wahrenberger, Angelia. "Pharmacologic immunosuppression." Critical Care Nursing Quarterly 17, no. 4 (February 1995): 27–36. http://dx.doi.org/10.1097/00002727-199502000-00006.

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Seton-Rogers, Sarah. "Dodging immunosuppression." Nature Reviews Cancer 16, no. 8 (July 25, 2016): 481. http://dx.doi.org/10.1038/nrc.2016.80.

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Kirk, Allan D. "Induction Immunosuppression." Transplantation 82, no. 5 (September 2006): 593–602. http://dx.doi.org/10.1097/01.tp.0000234905.56926.7f.

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Batiuk, Thomas D., Joan Urmson, Dianne Vincent, Randall W. Yatscoff, and Philip F. Halloran. "QUANTITATING IMMUNOSUPPRESSION." Transplantation 61, no. 11 (June 1996): 1618–24. http://dx.doi.org/10.1097/00007890-199606150-00012.

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Silkensen, John R., and Bertram L. Kasiske. "Immunosuppression withdrawal." Current Opinion in Organ Transplantation 6, no. 2 (June 2001): 169–74. http://dx.doi.org/10.1097/00075200-200106000-00012.

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Jolly, Elaine C., and Christopher J. E. Watson. "Modern immunosuppression." Surgery (Oxford) 29, no. 7 (July 2011): 312–18. http://dx.doi.org/10.1016/j.mpsur.2011.05.001.

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Figueiredo, Rodrigo S., and Colin Wilson. "Modern immunosuppression." Surgery (Oxford) 32, no. 7 (July 2014): 344–50. http://dx.doi.org/10.1016/j.mpsur.2014.04.014.

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Figueiredo, Rodrigo S., and Colin Wilson. "Modern immunosuppression." Surgery (Oxford) 35, no. 7 (July 2017): 353–59. http://dx.doi.org/10.1016/j.mpsur.2017.04.011.

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Leighton, James, and Colin Wilson. "Modern immunosuppression." Surgery (Oxford) 38, no. 7 (July 2020): 368–74. http://dx.doi.org/10.1016/j.mpsur.2020.04.005.

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