Relevant bibliographies by topics / Immunosuppression

Academic literature on the topic 'Immunosuppression'

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Published: 4 June 2021
Last updated: 30 July 2024

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Journal articles on the topic "Immunosuppression"

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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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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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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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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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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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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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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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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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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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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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Dissertations / Theses on the topic "Immunosuppression"

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Rodriguez, Grau Jorge Luis. "Suppression of Immune Functions by PCBs in the Earthworm Lumbricus terrestris." Thesis, University of North Texas, 1989. https://digital.library.unt.edu/ark:/67531/metadc798391/.

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This research is part of an effort to develop non-mammalian surrogate immunoessays with the earth worm Lumbricus terrestris to assess immunotoxic potential of xenobiotics to mammals. The objective was to determine if earthworm immunoessays, namely E- and S- rosette formation and phagocytosis, are sensitive to a known mammalian immunotoxin, the PCB Arclor 1254. Results are presented in terms of PCB exposure and tissue concentrations during uptake/depuration.
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Cousin, Céline. "Impact de l’enzyme Interleukin-4 induced gene 1 (IL4I1) sur les populations lymphocytaires T régulatrices." Thesis, Paris Est, 2014. http://www.theses.fr/2014PEST0026.

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Les travaux de l'équipe ont permis de montrer qu'IL4I1 est une L-amino acide oxydase sécrétée par les cellules d'origine myéloïde dégradant la phénylalanine en H2O2, NH3 et phénylpyruvate. Elle est fortement exprimée au sein des tumeurs humaines et facilite l'échappement tumoral dans un modèle de mélanome murin. Cette enzyme inhibe l'expression de la chaîne ζ du TCR ainsi que la prolifération des lymphocytes T effecteurs/mémoires via la production d'H2O2. IL4I1 appartient donc à une famille d'enzymes régulatrices des réponses immunitaires impliquées dans la défaillance de la réponse anti-tumorale.Au cours de ma thèse, j'ai montré qu'IL4I1 induit la différenciation des lymphocytes T CD4+ naïfs conventionnels en cellules CD25fortFoxP3+ chez l'Homme et la souris. Ces cellules exercent une action suppressive in vitro équivalente à celle de cellules régulatrices obtenues sans IL4I1 et leur phénotype est similaire. La promotion de la différenciation Treg par IL4I1 a pu être observée dans différentes conditions in vitro et s'avère particulièrement importante lorsque les cellules sont cultivées sans ajout d'IL2 et de TGFβ. Le mécanisme impliqué reposerait en partie sur la consommation de Phe par l'activité enzymatique qui serait responsable de l'inhibition de la voie mTORC1 observée.En conclusion, nous avons démontré un nouveau rôle d'IL4I1 sur les lymphocytes T. Ainsi, en inhibant la prolifération des lymphocytes T et en induisant la polarisation Treg, IL4I1 pourrait jouer un rôle important dans l'échappement tumoral. IL4I1 étant sécrétée et peu exprimée à l'état physiologique, elle pourrait être la cible de traitements adjuvants dans le cancer
Our team has shown that IL4I1 is a secreted L-amino acid oxidase which degrades phenylalanine into H2O2, NH3 and phenylpyruvate.. This enzyme is produced by myeloid cells and expressed within human cancers. IL4I1 expression facilitates tumor growth in a mouse model. IL4I1 inhibits TCRζ chain expression and T lymphocyte proliferation via H2O2 production. Therefore IL4I1 belongs to a family of enzymes endowed with immune regulatory functions involved in the anti-tumor response failure.During my PhD, I showed that IL4I1 induces CD25highFoxP3+ cells differentiation from conventional naïve CD4+ T cells, both in humans and mice in vitro systems. These cells exert similar in vitro suppressive activity than those obtained without IL4I1 with a similar phenotype. Treg differentiation promotion by L4I1 is observed in various in vitro conditions and is particularly important when cells are cultured without addition of IL2 and TGFβ. The involved mechanism would partially depend on the phenylalanine consumption by the enzymatic activity which would be responsible for the mTORC1 pathway inhibition observed.In conclusion, we have demonstrated a new mechanism of IL4I1 action on T lymphocytes. Thus, by inhibiting T lymphocytes proliferation and by inducing Treg polarization, IL4I1 could play an important role in tumor escape. Since IL4I1 is secreted and weakly expressed under physiological conditions, it could be the target of adjuvant therapy in cancer
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Brice, Sarah Louise, and sarahlbrice@gmail com. "Regional Immunosuppression for Corneal Transplantation." Flinders University. Medicine, 2010. http://catalogue.flinders.edu.au./local/adt/public/adt-SFU20100811.113448.

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Corneal transplantation is performed to restore vision or to relieve pain in patients with damaged or diseased corneas. However, approximately 40% of corneal allografts fail after 10 years. The most common cause of graft failure is irreversible immunological rejection, primarily mediated by CD4+ T cells, despite the topical application of glucocorticosteroids. The aim of this project was to investigate the anatomic site of antigen presentation during corneal transplantation in the rat, by using a lentiviral vector to express an anti-CD4 antibody fragment at potential sites of antigen presentation, including the donor corneal endothelium, the anterior segment of the eye and the cervical lymph nodes. Dual-gene lentiviral vectors were constructed by inserting the 2A self-processing sequence between two transgenes. This allowed expression of two transgenes within a single open reading frame. In vitro characterisation of the dual-gene vectors was performed in cell culture experiments, which showed that transgenic proteins were expressed at lower levels from dual-gene vectors compared to the expression from single-gene vectors and expression was lowest when the transgene was situated downstream of the 2A self-processing sequence. To locate the anatomic site of antigen presentation during corneal transplantation in rats, a lentiviral vector carrying an anti-CD4 antibody fragment was delivered to the corneal endothelium either immediately prior to corneal transplantation by ex vivo transduction of the donor corneas, or 5 days prior to corneal transplantation by anterior chamber injection into both the recipient and the donor rats. A separate group of recipient rats received intranodal injections of the lentiviral vector carrying an anti-CD4 antibody fragment into the cervical lymph nodes 2 days prior to corneal transplantation. Another group of rats underwent bilateral lymphadenectomy of the cervical lymph nodes 7 days prior to corneal transplantation. Corneal allografts were scored daily for opacity, inflammation and neovascularisation. Expression of the anti-CD4 antibody fragment from transduced tissues was detected using flow cytometry and polymerase chain reaction. Modest, but significant prolongation of corneal allograft survival was experienced by rats that received ex vivo transduction of the donor corneas with a lentiviral vector carrying an anti-CD4 antibody fragment immediately prior to corneal transplantation, but all grafts did eventually reject. Anterior chamber injection of the lentiviral vector carrying the anti-CD4 antibody fragment 5 days prior to corneal transplantation into both recipient and donor eyes did not prolong allograft survival. Intranodal injection of a lentiviral vector carrying an anti-CD4 antibody fragment did not prolong the survival of the corneal allografts, nor did bilateral lymphadenectomy of the cervical lymph nodes 7 days prior to corneal transplantation. Neither expression of the anti-CD4 antibody fragment in the cervical lymph nodes nor the removal of these nodes was able to prolong corneal allograft survival in rats, suggesting that T cell sensitisation could potentially occur elsewhere in the body. However, expression of the anti-CD4 antibody fragment from the donor corneal endothelium was able to prolong corneal allograft survival, suggesting that some antigen presentation might occur within the anterior segment of the eye. Based on the findings described in this thesis and those of others, I propose that antigen presentation in the rat occurs within anterior segment of the eye and within the secondary lymphoid tissues such as the cervical lymph nodes, and that inhibiting antigen presentation at one of these sites will delay graft rejection. However, to completely abolish antigen presentation during corneal transplantation in the rat, I hypothesise that antigen presentation within both the anterior segment of the eye and within the secondary lymphoid tissues must be inhibited.
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Ruers, Theodoor Jacques Marie. "Selective immunosuppression in organ transplantation." Maastricht : Maastricht : Rijksuniversiteit Limburg ; University Library, Maastricht University [Host], 1989. http://arno.unimaas.nl/show.cgi?fid=5415.

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Thompson, Rebecca Lynn. "Steroid induced immunosuppression and alternative male reproductive strategies /." Digital version accessible at:, 1998. http://wwwlib.umi.com/cr/utexas/main.

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Pers, Yves-Marie. "Effet thérapeutique des cellules souches mésenchymateuses dans l'arthrose : mécanismes et translation clinique." Thesis, Montpellier, 2018. http://www.theses.fr/2018MONTT045.

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Les cellules souches mésenchymateuses (CSM) sont des cellules stromales présentes dans différents types de tissus. En plus de leur capacité à se différencier en plusieurs lignées (chondrocytes, adipocytes et ostéoblastes), les CSM présentent également des propriétés immunosuppressives. Bien que ces mécanismes soient loin d'être entièrement compris, leur capacité immunosuppressive a récemment été démontrée comme étant modulée par des miARN. L'arthrose est la forme la plus courante de maladies articulaires sans traitement curatif et se caractérise principalement par la dégradation du cartilage articulaire, avec des altérations osseuses sous-chondrales et une inflammation synoviale. Les CSM pourraient offrir un potentiel thérapeutique intéressant pour le traitement de l'arthrose.Nos travaux ont montré qu'une injection autologue de CSM d'origine adipeuse (ASC) dans une articulation arthrosique améliore la douleur et les niveaux fonctionnels chez les patients. Nous avons souligné la tolérance immunitaire systémique induite à la suite d'injections intra-articulaires d'ASC. Enfin, nous avons étudié le profil d'expression des miARN des CSM humaines lors de leur stimulation par des cellules mononuclées du sang préalablement activés. Nous avons identifié le miR-29a et le PSAT1 comme de nouveaux candidats pour réguler l'activité immunosuppressive médiée par les CSM
Mesenchymal Stem Cells (MSCs) are stromal cells present in a number of different tissue types. In addition to their ability to differentiate into multiple lineages (chondrocytes, adipocytes and osteoblasts), MSCs also display immunosuppressive properties. Whilst these mechanisms are far from fully understood, their immunosuppressive capacity has recently been shown to be modulated by miRNAs. OA is the most common form of joint diseases without curative treatment and mainly characterized by the degradation of articular cartilage, with subchondral bone alterations and synovial inflammation. MSC might provide therapeutic potential for treatment of OA.Here, we showed that an autologous injection of adipose-derived MSC (ASC) into an osteoarthritic joint improved pain and function levels in patients. We underscored the systemic immune tolerance induced following intra-articular injections of ASCs. Finally, we investigated the miRNA expression profile of human MSCs upon their stimulation by peripheral blood mononuclear cells. We identified miR-29a and PSAT1 as new candidates to regulate immunosuppressive activity mediated by MSCs
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Ruglys, M. P. "Studies on immunosuppression in teleost fish." Thesis, University of Hull, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.377400.

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Quayle, Alison Jane. "Studies on immunosuppression by seminal plasma." Thesis, University of Edinburgh, 1988. http://hdl.handle.net/1842/19250.

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Honey, C. R. "Immunosuppression with monoclonal antibodies in neural transplantation." Thesis, University of Oxford, 1990. http://ora.ox.ac.uk/objects/uuid:ea39dc7a-4ada-4c21-8cef-4649cb322646.

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Heaney, J. "Immunosuppression and virus-cell interactions in morbilliviruses." Thesis, Queen's University Belfast, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.246332.

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Books on the topic "Immunosuppression"

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Thomson, Angus W., ed. Therapeutic Immunosuppression. Dordrecht: Springer Netherlands, 2001. http://dx.doi.org/10.1007/978-94-010-0765-8.

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Eisen, Howard J., ed. Pharmacology of Immunosuppression. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-05118-0.

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Cochat, P., J. Traeger, C. Merieux, and M. Derchavane, eds. Immunosuppression under Trial. Dordrecht: Springer Netherlands, 1999. http://dx.doi.org/10.1007/978-94-011-4643-2.

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Specter, Steven, Mauro Bendinelli, and Herman Friedman, eds. Virus-Induced Immunosuppression. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-5583-0.

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Taylor, Charles B. Immunosuppression: New research. New York: Nova Biomedical Books, 2009.

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Steven, Specter, Bendinelli Mauro, and Friedman Herman 1931-, eds. Virus-induced immunosuppression. New York: Plenum Press, 1989.

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Naor, David, Benjamin Y. Klein, Nora Tarcic, and Jonathan S. Duke-Cohan. Immunosuppression and Human Malignancy. Totowa, NJ: Humana Press, 1990. http://dx.doi.org/10.1007/978-1-4612-4496-7.

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David, Naor, ed. Immunosuppression and human malignancy. Clifton, N.J: Humana Press, 1989.

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W, Thomson Angus, ed. The Molecular biology of immunosuppression. Chichester: Wiley, 1992.

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Gruber, Scott A. Local Immunosuppression of Organ Transplants. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-662-22105-1.

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Book chapters on the topic "Immunosuppression"

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Citerio, G., C. Giussani, Hugo Sax, Didier Pittet, Xiaoyan Wen, John A. Kellum, Angela M. Mills, et al. "Immunosuppression." In Encyclopedia of Intensive Care Medicine, 1206–12. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-00418-6_294.

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MacPhee, Iain A. M., and Teun van Gelder. "Immunosuppression." In Handbook of Renal and Pancreatic Transplantation, 243–70. Chichester, UK: John Wiley & Sons, Ltd, 2012. http://dx.doi.org/10.1002/9781118305294.ch16.

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White, D. J. G., P. Friend, and R. Y. Calne. "Immunosuppression." In Transplantation, 117–33. Dordrecht: Springer Netherlands, 1989. http://dx.doi.org/10.1007/978-94-009-0855-0_5.

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Geissler, Edward K. "Immunosuppression." In Skin Cancer after Organ Transplantation, 23–43. Boston, MA: Springer US, 2009. http://dx.doi.org/10.1007/978-0-387-78574-5_4.

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McGeown, Mary G. "Immunosuppression." In Clinical Management of Renal Transplantation, 201–29. Dordrecht: Springer Netherlands, 1992. http://dx.doi.org/10.1007/978-94-015-7961-2_15.

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Gonsalkorala, Enoka, Daphne Hotho, and Kosh Agarwal. "Immunosuppression." In Liver Anesthesiology and Critical Care Medicine, 431–44. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-64298-7_32.

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McMaster, Paul. "Immunosuppression." In Pancreas Transplantation, 189–202. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4613-1735-7_11.

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Drews, Jürgen. "Immunosuppression." In Immunopharmacology, 129–64. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-75561-3_4.

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Gooch, Jan W. "Immunosuppression." In Encyclopedic Dictionary of Polymers, 901. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_14001.

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Cruse, Julius M., and Robert E. Lewis. "Immunosuppression." In Atlas of Immunology, 345–52. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-662-11196-3_19.

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Conference papers on the topic "Immunosuppression"

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Mackay, Alexander J., Stephen Burke, and Graham Bothamley. "Resurrection With Immunosuppression: Dermatomyositis Sine Dermatosis." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2940.

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Bellon, Hannelore, Elly Vandermeulen, Stijn Verleden, David Ruttens, Hanne Vriens, Hoet Peter, Bart Vanaudenaerde, Robin Vos, and Geert Verleden. "The effect of immunosuppression on airway integrity." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa1799.

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Shah, Shivanee, Rudolf Braun, Alicia Martin, Melissa Medina, Robert B. Love, and Makio Iwashima. "Omental Cells: A Novel Approach To Immunosuppression." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2764.

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Zacarin, Maria Fernanda, Régis Suwa Marques, Rodrigo da Rocha Jorge, Vítor de Castro Grotti, Thaís Cristina Faria Pacheco, Gabrielle Avelar Lamoglia Lopes, Thiago Junqueira Trevisan, Ana Paula Toledo Del Rio, Manoel Barros Bertolo, and Alisson Aliel Vigano Pugliesi. "FUNGAL OSTEOMYELITIS IN THE CONTEXT OF IMMUNOSUPPRESSION." In XXXIX Congresso Brasileiro de Reumatologia. Sociedade Brasileiro de Reumatologia, 2022. http://dx.doi.org/10.47660/cbr.2022.2082.

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Petri, Michelle, Daniel Joyce, Kristin Haag, Andrea Fava, Daniel W. Goldman, Diana Zhong, Shaoming Shao, Aaron Milstone, and Laurence S. Magder. "627 Effect of Immunosuppression on COVID Vaccination." In LUPUS 21ST CENTURY 2022 CONFERENCE, Abstracts of Sixth Scientific Meeting of North American and European Lupus Community, Tucson, AZ, USA – September 20–23, 2022. Lupus Foundation of America, 2022. http://dx.doi.org/10.1136/lupus-2022-lupus21century.48.

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Tejera Quesada, C., J. Baek, R. Reddy, A. Rodriguez, and G. Avila Amat. "Immunosuppression: A Hidden Component of Virchows' Triad." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a1819.

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Psalms, K., and B. Silverman. "Chronic Bronchitis Induced by Immunosuppression from Betalacept." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a2817.

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Kemp, K., F. Birchall, H. Dutton, M. Kirkbride, J. Brooks, and S. Levison. "OC-035 Streamlining immunosuppression therapy and improving the quality of care for ibd patients: a virtual immunosuppression clinic." In British Society of Gastroenterology, Annual General Meeting, 19–22 June 2017, Abstracts. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2017. http://dx.doi.org/10.1136/gutjnl-2017-314472.35.

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Matucci-Cerinic, Marco. "SP0112 IMMUNOSUPPRESSION – ONE FITS ALL VS. INDIVIDUALIZED SELECTION?" In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.8534.

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Nejo, Takahide, Saritha Krishna, Akane Yamamichi, Christian Jimenez, Jacob S. Young, Senthilnath Lakshmanachetty, Tiffany Chen, et al. "956 Glioma-neuronal circuit remodeling induces regional immunosuppression." In SITC 38th Annual Meeting (SITC 2023) Abstracts. BMJ Publishing Group Ltd, 2023. http://dx.doi.org/10.1136/jitc-2023-sitc2023.0956.

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Reports on the topic "Immunosuppression"

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Weyant, Debra. Androgen-induced immunosuppression. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.2791.

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Chejanovsky, Nor, and Bruce A. Webb. Potentiation of Pest Control by Insect Immunosuppression. United States Department of Agriculture, January 2010. http://dx.doi.org/10.32747/2010.7592113.bard.

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The restricted host range of many baculoviruses, highly pathogenic to Lepidoptera and non-pathogenic to mammals, limits their use to single or few closely related Lepidopteran species and is an obstacle to extending their implementation for pest control. The insect immune response is a major determinant of the ability of an insect pathogen to efficiently multiply and propagate. We have developed an original model system to study the Lepidopteran antiviral immune response based on Spodoptera littoralis resistance to AcMNPV (Autographa californica multiple nucleopolyhedrovirus) infection and the fascinating immunosuppressive activity of polydnaviruses .Our aim is to elucidate the mechanisms through which the immunosuppressive insect polydnaviruses promote replication of pathogenic baculoviruses in lepidopteran hosts that are mildly or non-permissive to virus- replication. In this study we : 1- Assessed the extent to which and the mechanisms whereby the immunosuppressive Campoletis sonorensis polydnavirus (CsV) or its genes enhanced replication of a well-characterized pathogenic baculovirus AcMNPV, in polydnavirus-immunosuppressedH. zea and S. littoralis insects and S. littoralis cells, hosts that are mildly or non-permissive to AcMNPV. 2- Identified CsV genes involved in the above immunosuppression (e.g. inhibiting cellular encapsulation and disrupting humoral immunity). We showed that: 1. S. littoralis larvae mount an immune response against a baculovirus infection. 2. Immunosuppression of an insect pest improves the ability of a viral pathogen, the baculovirus AcMNPV, to infect the pest. 3. For the first time two PDV-specific genes of the vankyrin and cystein rich-motif families involved in immunosuppression of the host, namely Pvank1 and Hv1.1 respectively, enhanced the efficacy of an insect pathogen toward a semipermissive pest. 4. Pvank1 inhibits apoptosis of Spodopteran cells elucidating one functional aspect of PDVvankyrins. 5. That Pvank-1 and Hv1.1 do not show cooperative effect in S. littoralis when co-expressed during AcMNPV infection. Our results pave the way to developing novel means for pest control, including baculoviruses, that rely upon suppressing host immune systems by strategically weakening insect defenses to improve pathogen (i.e. biocontrol agent) infection and virulence. Also, we expect that the above result will help to develop systems for enhanced insect control that may ultimately help to reduce transmission of insect vectored diseases of humans, animals and plants as well as provide mechanisms for suppression of insect populations that damage crop plants by direct feeding.
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Chejanovsky, Nor, and Bruce A. Webb. Potentiation of pest control by insect immunosuppression. United States Department of Agriculture, July 2004. http://dx.doi.org/10.32747/2004.7587236.bard.

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Our original aims were to elucidate the mechanisms through which the immunosuppressive insect virus, the Campoletis sonorensis polydnavirus (CsV) promotes replication of a well-characterized pathogenic virus, the Autographa californica multiple nucleopolyhedrovirus (AcMNPV) in hosts that are mildly or non-permissive to virus replication. According to the BARD panels criticism we modified our short-term goals (see below). Thus, in this feasibility study (one-year funding) we aimed to show that: 1. S. littoralis larvae mount an immune response against a baculovirus infection. 2. Immunosuppression of an insect pest improves the ability of a viral pathogen (a baculovirus) to infect the pest. 3. S. littoralis cells constitute an efficient tool to study some aspects of the anti- viral immune response. We achieved the above objectives by: 1. Finding melanized viral foci upon following the baculoviral infection in S . littoralis larvae infected with a polyhedra - positive AcMNPV recombinant that expressed the GFP gene under the control of the Drosophila heat shock promoter. 2. Studying the effect of AcMNPV-infection in S . littoralis immunosuppressed by parasitation with the Braconidae wasp Chelonus inanitus that bears the CiV polydna virus, that resulted in higher susceptibility of S. littoralis to AcMNPV- infection. 3. Proving that S. littoralis hemocytes resist AcMNPV -infection. 4. Defining SL2 as a granulocyte-like cell line and demonstrating that as littoralis hemocytic cell line undergoes apoptosis upon AcMNPV -infection. 5. Showing that some of the recombinant AcMNPV expressing the immuno-suppressive polydna virus CsV- vankyrin genes inhibit baculoviral-induced lysis of SL2 cells. This information paves the way to elucidate the mechanisms through which the immuno- suppressive polydna insect viruses promote replication of pathogenic baculoviruses in lepidopteran hosts that are mildly or non-permissive to virus- replication by: - Assessing the extent to which and the mechanisms whereby the immunosuppressive viruses, CiV and CsV or their genes enhance AcMNPV replication in polydnavirus- immunosuppressed H. zea and S. littoralis insects and S. littoralis cells. - Identifying CiV and CsV genes involved in the above immunosuppression (e.g. inhibiting cellular encapsulation and disrupting humoral immunity). This study will provide insight to the molecular mechanisms of viral pathogenesis and improve our understanding of insect immunity. This knowledge is of fundamental importance to controlling insect vectored diseases of humans, animals and plants and essential to developing novel means for pest control (including baculoviruses) that strategically weaken insect defenses to improve pathogen (i.e. biocontrol agent) infection and virulence.
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Schat, Karel Antoni, Irit Davidson, and Dan Heller. Chicken infectious anemia virus: immunosuppression, transmission and impact on other diseases. United States Department of Agriculture, 2008. http://dx.doi.org/10.32747/2008.7695591.bard.

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1. Original Objectives. The original broad objectives of the grant were to determine A) the impact of CAV on the generation of cytotoxic T lymphocytes (CTL) to reticuloendotheliosis virus (REV) (CU), B). the interactions between chicken anemia virus (CAV) and Marek’s disease virus (MDV) with an emphasis on horizontal spread of CAV through feathers (KVI), and C) the impact of CAV infection on Salmonella typhimurium (STM) (HUJI). During the third year and the one year no cost extension the CU group included some work on the development of an antigen-antibody complex vaccine for CAV, which was partially funded by the US Poultry and Egg Association. 2. Background to the topic. CAV is a major pathogen causing clinical disease if maternal antibody-free chickens are infected vertically or horizontally between 1 and 14 days of age. Infection after 3 weeks of age when maternal antibodies are not longer present can cause severe subclinical immunosuppression affecting CTL and cytokine expression. The subclinical immunosuppression can aggravate many diseases including Marek’s disease (MD) and several bacterial infections. 3. Major conclusions and achievements. The overall project contributed in the following ways to the knowledge about CAV infection in poultry. As expected CAV infections occur frequently in Israel causing problems to the industry. To control subclinical infections vaccination may be needed and our work indicates that the development of an antigen-antibody complex vaccine is feasible. It was previously known that CAV can spread vertically and horizontally, but the exact routes of the latter had not been confirmed. Our results clearly show that CAV can be shed into the environment through feathers. A potential interaction between CAV and MD virus (MDV) in the feathers was noted which may interfere with MDV replication. It was also learned that inoculation of 7-day-old embryos causes growth retardation and lesions. The potential of CAV to cause immunosuppression was further examined using CTL responses to REV. CTL were obtained from chickens between 36 and 44 days of age with REV and CAV given at different time points. In contrast to our earlier studies, in these experiments we were unable to detect a direct impact of CAV on REV-specific CTL, perhaps because the CTL were obtained from older birds. Inoculation of CAV at one day of age decreased the IgG antibody responses to inactivated STM administered at 10 days of age. 4. Scientific and Agricultural Implications The impact of the research was especially important for the poultry industry in Israel. The producers have been educated on the importance of the disease through the many presentations. It is now well known to the stakeholders that CAV can aggravate other diseases, decrease productivity and profitability. As a consequence they monitor the antibody status of the breeders so that the maternal antibody status of the broilers is known. Also vaccination of breeder flock that remain antibody negative may become feasible further reducing the negative impact of CAV infection. Vaccination may become more important because improved biosecurity of the breeder flocks to prevent avian influenza and Salmonella may delay the onset of seroconversion for CAV by natural exposure resulting in CAV susceptible broilers lacking maternal antibodies. Scientifically, the research added important information on the horizontal spread of CAV through feathers, the interactions with Salmonella typhimurium and the demonstration that antigen-antibody complex vaccines may provide protective immunity.
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Zhang, Gongming, Binwei Duan, and Guangming Li. The efficacy of mTORi based immunosuppression In Liver Transplantation: A Systematic Review and Meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, January 2022. http://dx.doi.org/10.37766/inplasy2022.1.0058.

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Pelletier, Joseph P., Oluwole Fadare, and Yanyun Wu. Post-Renal Transplant Thrombotic Thrombocytopenic Purpura (TTP): Attributable to Immunosuppression or Graft Rejection? Report of Three Cases and Literature Review. Fort Belvoir, VA: Defense Technical Information Center, January 2005. http://dx.doi.org/10.21236/ada429608.

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Yang, Ming, Youwei Wu, Tao Wang, and Wentao Wang. Iron overload, Infectious Complications and Survival In Liver Transplant Recipients: A Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2022. http://dx.doi.org/10.37766/inplasy2022.11.0022.

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Review question / Objective: Iron overload conditions is a well-established risk factor for infection of pathogens. The possible association of iron overload with infectious complications and prognosis of patients receiving transplants are not well understood. Condition being studied: Liver transplantation often represents a life-saving treatment for an increasing number of patients with end-stage liver disease. With the improvements in surgical techniques, immunosuppression strategies, and post-LT management of complications, the recipient mortality has steadily declined after LT. The survival rates were 83% at 1 year, 71% at 5 years in western countries. However, the use of immunosuppressants increased risk of infections as an adverse effect resulting in severe morbidity. Globally, infection caused by including bacteria, fungus, viruses remain one of the leading causes of morbidity and mortality among transplant recipients. Knowledge of modifiable risk factors and potentially reversible causes is essential to develop targeted preventive strategies.
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Malkinson, Mertyn, Richard Witter, and Irit Davidson. Reduction of Reticuloendotheliosis in Foundation Breeding Flocks of Chickens: A Combined Immunological and Molecular Biological Approach. United States Department of Agriculture, February 1996. http://dx.doi.org/10.32747/1996.7613026.bard.

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Reticuloendotheliosis virus (REV) is an avian retrovirus that can cause immunosuppression, growth retardation and tumors. An attempt to define the extent of the economic damage to the poultry industry that it causes is discussed in this report. In addition to losses experienced by commercial laying flocks, reduced rates of hatchability and embryo developmental disorders were demonstrable due to vertical transmission of the virus. I. Eradication of REV In this project a comprehensive national program was applied for the eradication of REV from Israeli breeding stocks by the elimination of antibody-positive birds from the breeding program. The prevention of REV-infected breeders entering Israel was also implemented by serological examination of imported day-old chickens and turkeys for maternal antibody. At the same time commercial breeding flocks in Israel were surveyed routinely to measure the extent of environmental exposure to REV throughout Israel. II. Economic factors associated with vertical transmission on breeders and progeny It was observed that on some poultry farms exposure of breeding flocks to viral infection, if it occurs when the birds are immunocompetent, leads only to a seroconvertion event. In these flocks no differences were demonstrated between the performances of seronegative and seropositive birds. When the F1 generation was selected according to seronegativity of the parents, all the progeny were seronegative, indicating that tolerantly infected birds did not form a significant proportion of the parent flock. In sharp contrast, breeding flocks that became exposed to the virus about the point of lay or during the laying period, shed virus vertically for a brief period of time through the egg. Our epizootiological observations lead us to conclude that the progeny (laying pullets) becomes tolerantly infected and are immunosuppressed as they increase in age. Increased mortality and susceptibility to intercurrent diseases were recorded.
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Hui, Xu. Enhancement of Tumor Immunotherapy by Blockade of a Prostate Tumor Derived Immunosuppressive Factor. Fort Belvoir, VA: Defense Technical Information Center, August 2006. http://dx.doi.org/10.21236/ada462748.

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Yusup, Muyassar, JianPing Hao, GuangSheng He, Niluopaer Tuerxun, and YuTing Qin. Efficacy and influencing factors of most prevalent immunosuppressive therapy for pure red cell aplasia:meta-analysis and systematic review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, April 2024. http://dx.doi.org/10.37766/inplasy2024.4.0070.

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