Academic literature on the topic 'Graft rejection; Tumours; Autoimmune diseases'
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Journal articles on the topic "Graft rejection; Tumours; Autoimmune diseases"
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Lee, Gap Ryol. "Phenotypic and Functional Properties of Tumor-Infiltrating Regulatory T Cells." Mediators of Inflammation 2017 (2017): 1–9. http://dx.doi.org/10.1155/2017/5458178.
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Regulatory T (Treg) cells maintain immune homeostasis by suppressing excessive immune responses. Treg cells induce tolerance against self- and foreign antigens, thus preventing autoimmunity, allergy, graft rejection, and fetus rejection during pregnancy. However, Treg cells also infiltrate into tumors and inhibit antitumor immune responses, thus inhibiting anticancer therapy. Depleting whole Treg cell populations in the body to enhance anticancer treatments will produce deleterious autoimmune diseases. Therefore, understanding the precise nature of tumor-infiltrating Treg cells is essential for effectively targeting Treg cells in tumors. This review summarizes recent results relating to Treg cells in the tumor microenvironment, with particular emphasis on their accumulation, phenotypic, and functional properties, and targeting to enhance the efficacy of anticancer treatment.
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Storb, Rainer F., Guido Lucarelli, Peter A. McSweeney, and Richard W. Childs. "Hematopoietic Cell Transplantation for Benign Hematological Disorders and Solid Tumors." Hematology 2003, no. 1 (January 1, 2003): 372–97. http://dx.doi.org/10.1182/asheducation.v2003.1.372.0010372.
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Allogeneic hematopoietic cell transplantation (HCT) has been successfully used as replacement therapy for patients with aplastic anemia and hemoglobinopathies. Both autologous and allogeneic HCT following high-dose chemotherapy can correct manifestations of autoimmune diseases. The impressive allogeneic graft-versus-tumor effects seen in patients given HCT for hematological malignancies have stimulated trials of allogeneic immunotherapy in patients with otherwise refractory metastatic solid tumors. This session will update the status of HCT in the treatment of benign hematological diseases and solid tumors. In Section I, Dr. Rainer Storb reviews the development of nonmyeloablative conditioning for patients with severe aplastic anemia who have HLA-matched family members. He also describes the results in patients with aplastic anemia given HCT from unrelated donors after failure of responding to immunosuppressive therapy. The importance of leuko-poor and in vitro irradiated blood product transfusions for avoiding graft rejection will be discussed. In Section II, Dr. Guido Lucarelli reviews the status of marrow transplantation for thalassemia major and updates results obtained in children with class I and class II severity of thalassemia. He also describes results of new protocols for class III patients and efforts to extend HCT to thalassemic patients without HLA-matched family members. In Section III, Dr. Peter McSweeney reviews the current status of HCT for severe autoimmune diseases. He summarizes the results of autologous HCT for systemic sclerosis, multiple sclerosis, rheumatoid arthritis, and systemic lupus erythematosus, and reviews the status of planned Phase III studies for autologous HCT for these diseases in North America and Europe. He also discusses a possible role of allogeneic HCT in the treatment of these diseases. In Section IV, Dr. Richard Childs discusses the development and application of nonmyeloablative HCT as allogeneic immunotherapy for treatment-refractory solid tumors. He reviews the results of pilot clinical trials demonstrating graft-versus-solid tumor effects in a variety of metastatic cancers and describes efforts to characterize the immune cell populations mediating these effects, as well as newer methods to target the donor immune system to the tumor.
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Storb, Rainer F., Guido Lucarelli, Peter A. McSweeney, and Richard W. Childs. "Hematopoietic Cell Transplantation for Benign Hematological Disorders and Solid Tumors." Hematology 2003, no. 1 (January 1, 2003): 372–97. http://dx.doi.org/10.1182/asheducation-2003.1.372.
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Abstract Allogeneic hematopoietic cell transplantation (HCT) has been successfully used as replacement therapy for patients with aplastic anemia and hemoglobinopathies. Both autologous and allogeneic HCT following high-dose chemotherapy can correct manifestations of autoimmune diseases. The impressive allogeneic graft-versus-tumor effects seen in patients given HCT for hematological malignancies have stimulated trials of allogeneic immunotherapy in patients with otherwise refractory metastatic solid tumors. This session will update the status of HCT in the treatment of benign hematological diseases and solid tumors. In Section I, Dr. Rainer Storb reviews the development of nonmyeloablative conditioning for patients with severe aplastic anemia who have HLA-matched family members. He also describes the results in patients with aplastic anemia given HCT from unrelated donors after failure of responding to immunosuppressive therapy. The importance of leuko-poor and in vitro irradiated blood product transfusions for avoiding graft rejection will be discussed. In Section II, Dr. Guido Lucarelli reviews the status of marrow transplantation for thalassemia major and updates results obtained in children with class I and class II severity of thalassemia. He also describes results of new protocols for class III patients and efforts to extend HCT to thalassemic patients without HLA-matched family members. In Section III, Dr. Peter McSweeney reviews the current status of HCT for severe autoimmune diseases. He summarizes the results of autologous HCT for systemic sclerosis, multiple sclerosis, rheumatoid arthritis, and systemic lupus erythematosus, and reviews the status of planned Phase III studies for autologous HCT for these diseases in North America and Europe. He also discusses a possible role of allogeneic HCT in the treatment of these diseases. In Section IV, Dr. Richard Childs discusses the development and application of nonmyeloablative HCT as allogeneic immunotherapy for treatment-refractory solid tumors. He reviews the results of pilot clinical trials demonstrating graft-versus-solid tumor effects in a variety of metastatic cancers and describes efforts to characterize the immune cell populations mediating these effects, as well as newer methods to target the donor immune system to the tumor.
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Im, Ho Joon, Kyung Nam Koh, Jin Kyung Suh, Eun Seok Choi, Seongsoo Jang, Chan-Jeoung Park, and Jong Jin Seo. "Haploidentical Hematopoietic Stem Cell Transplantation in Pediatric Patients: Comparison of Early Post-Transplant Outcome According to in Vitro Depletion Method." Blood 124, no. 21 (December 6, 2014): 1229. http://dx.doi.org/10.1182/blood.v124.21.1229.1229.
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Abstract Currently, haploidentical hematopoietic cell transplantation (HHCT) is considered an established option for patients who have diseases curable with HCT but who lack a suitable donor. We compared the early post-transplant outcomes of the two transplant groups using different in vitro depletion method. Between July 2008 and June 2014, 49 pediatric patients underwent in vitro T cell-depleted HHCT. Of 49 patients, 28 received CD3-depleted stem cells (CD3-HHCT) and 21 received TCRαβ-depleted grafts (TCRαβ-HHCT). Among 28 patients of CD3-HHCT, nine had hematologic malignancy [HM, one with ALL in non-CR, six with AML (3 CR1, 2 CR2, 1 non-CR), and two with MDS-RCMD], 18 had non-malignant disease (one with Fanconi anemia, 16 with acquired SAA, and one with CDA), and one had refractory neuroblastoma. Among 21 patients of TCRαβ-HHCT, 16 had HM [five with ALL (2 CR1, 2 CR2, 1 CR3), five with AML (2 CR1, 2 CR2, 1 non-CR), one with mixed lineage leukemia in non-CR, one with MDS-RCC, two with JMML, and two with NHL (1 CR2, 1 CR3)], two had SAA, and three had solid tumors [two with RMS (1 CR2, 1 refractory), and one with Ewing sarcoma in CR3]. Of 28 patients who received CD3-HHCT, two patients failed to achieve primary engraftment, and five patients experienced graft rejection (GR) within 28 days post-transplant. No patients of TCRαβ-HHCT experienced graft failure (GF). Early GF (primary GF and GR) was more common in CD3-HHCT compared to TCRαβ-HHCT (P=0.011). The cumulative incidence of acute GVHD ≥ grade II was comparable between two groups (33.3% for CD3-HHCT and 27.0% for TCRαβ-HHCT). Extensive chronic GVHD occurred in three patients from CD3-HHCT and one from TCRαβ-HHCT. T and T4 cell counts at 2 months post-transplant were higher in TCRαβ-HHCT than that of CD3-HHCT (P=0.007 for T and P=0.074 for T4). In CD3-HHCT, four patients died of non-relapse causes (two of CMV disease, one of encephalopathy, and one of autoimmune hemolytic anemia) and one died of leukemia. In contrast, five patients from TCRαβ-HHCT died of disease but, none died of non-relapse cause. Of 20 patients (18 from CD3-HHCT and two from TCRαβ-HHCT) with non-malignant disease, only one patient of CD3-HHCT died of TRM. As for 29 patients (10 from CD3-HHCT and 19 from TCRαβ-HHCT) with malignant disease, the EFS at 1 year for CD3-HHCT and TCRαβ-HHCT were 60.0% and 56.6%, respectively (P>0.05). In this study, TCRαβ-depleted HHCT showed a better early post-transplant outcome in terms of engraftment, immune recovery, and NRM, compared to CD3-HHCT. However, further study is warranted to evaluate the efficacy of TCRαβ-HHCT in preventing relapse in advanced malignancy. Disclosures No relevant conflicts of interest to declare.
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Emerson, Amy E., Emily M. Slaby, Shivani C. Hiremath, and Jessica D. Weaver. "Biomaterial-based approaches to engineering immune tolerance." Biomaterials Science 8, no. 24 (2020): 7014–32. http://dx.doi.org/10.1039/d0bm01171a.
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Bordron, A., A. Mankaï, B. Bendaoud, A. Saraux, V. Devauchelle, I. Ghedira, C. Jamin, J. C. Pers, C. Berthou, and P. Youinou. "B Cell-Ablative Therapy: Where are We Now?" International Journal of Immunopathology and Pharmacology 20, no. 4 (October 2007): 655–59. http://dx.doi.org/10.1177/039463200702000401.
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Based on their multifaceted functions, B cells participate in several pathological settings such as lymphoproliferative disorders, autoimmune diseases and graft rejection. B cell-ablative therapy has thus emerged as a mainstay in these diseases. A number of anti-B cell antibodies (Abs) have been generated, among which anti-CD20 Abs appear to be efficient. Rituximab (RTX) is one of these anti-CD20 monoclonal Abs. Originally approved for the treatment of non-Hodgkin lymphoma, RTX is now being administered in other malignant proliferations, applied to an increasing number of autoimmune diseases and required to prevent rejection of a graft. Although this medication is remarkably safe, a handful of laboratory tests have been proposed to monitor RTX-treated patients. The efficacy in different diseases, and the emergence of new anti-CD20 Abs raise many questions. Thus, their detailed understanding can lead to a better issue for inhibition of immune responses.
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Niemand, Claudia, Carina Conrads, Ramona Siemer, and Mario Assenmacher. "Rapid Clinical Scale Isolation of CD25hiCD4+ Regulatory T Cells." Blood 104, no. 11 (November 16, 2004): 4969. http://dx.doi.org/10.1182/blood.v104.11.4969.4969.
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Abstract Several publications during the last few years have reported CD25hiCD4+ regulatory T cells (Tregs) to prevent or to reverse disease in different mouse models of experimental autoimmune encephalomyelitis (EAE), colitis, graft rejection and graft-versus-host-disease (GvHD). As mouse and human Tregs share many phenotypical and functional characteristics, Tregs could provide a promising therapeutic approach for various human autoimmune diseases and pathological alloresponses. Here we have shown that Tregs can be isolated from leukapheresis harvests by CD25 enrichment using the CliniMACS technology (n=13). By this procedure we obtained 2.32x108 (± 1.12x108, range 0.71–4.42x108) cells out of 1010 mononuclear cells with a mean purity of 52.12% (± 12.11%, range 25.48–66.61%) for CD25hiCD4+ cells. Around 90% of enriched cells were CD25+CD4+. Among contaminating CD4− cells most cells were CD25+ which were further characterized by counterstaining to be mainly CD19+ B cells and a few CD8+, CD56+ or CD123+ cells. It is possible to deplete the CD19+ or CD8+ cells by using CD19 Microbeads or CD8 Microbeads respectively with the CliniMACS Instrument before CD25 enrichment. Combined depletion of different cells, e.g. CD19+ and CD8+ cells is conceivable. Isolated cells were phenotypically and functionally characterized. The majority of the CD25hiCD4+ T cells expressed glucocorticoid-induced tumor necrosis factor receptor (GITR), CD62L and CD45RO. In addition, isolated cells were able to suppress the proliferation and activation of cocultured conventional CD4+ cells after polyclonal stimulation with anti-CD3 antibody. We conclude that the large-scale isolation of CD25hiCD4+ regulatory T cells for clinical applications (e.g. therapy of autoimmune diseases, graft rejection or GvHD) is possible by using the CliniMACS CD25 Reagent and the CliniMACS Instrument.
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Jenh, Chung-Her, Mary Ann Cox, Long Cui, Eva-Pia Reich, Lee Sullivan, Shu-Cheng Chen, David Kinsley, et al. "A selective and potent CXCR3 antagonist SCH 546738 attenuates the development of autoimmune diseases and delays graft rejection." BMC Immunology 13, no. 1 (2012): 2. http://dx.doi.org/10.1186/1471-2172-13-2.
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Kaouther, Mnasria, and Oueslati Ridha. "Dendritic Cell-Based Graft Tolerance." ISRN Pharmacology 2011 (April 10, 2011): 1–4. http://dx.doi.org/10.5402/2011/347134.
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It has recently been demonstrated that mouse and human dendritic cells (DCs) can produce IL-2 after activation. However the role of the IL2/IL2R pathway in DC functions has not yet been fully elucidated. The results presented in this study provide several new insights into the role of this pathway in DCs. We report that stimulation of human monocyte-derived DCs with LPS strongly upregulated CD25 (α chain of the IL2R) expression. In additon, by using a humanized monoclonal antibody against CD25, we demonstrated that the IL2 signalling in DC upregulated both IL-12 and γIFN production but decreased IL10 synthesis. We also found that LPS-matured DCs produced IL2. Taken together, these results suggest that IL-2 actively contributes to the DC activation through an autocrine pathway. Furthermore, our results indicate that the IL2 pathway in DC is involved in the development of T-helper priming ability and in the upregulation of surface markers characteristic of a “mature” phenotype. This study therefore provide new molecular clues regarding the split between these two phenomena and unravel new mechanisms of action of anti-CD25 monoclonal antibodies that may contribute to their action in several human immunological disorders such as autoimmune diseases and acute allograft rejection.
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Zulpaite, Ruta, Povilas Miknevicius, Bettina Leber, Kestutis Strupas, Philipp Stiegler, and Peter Schemmer. "Tryptophan Metabolism via Kynurenine Pathway: Role in Solid Organ Transplantation." International Journal of Molecular Sciences 22, no. 4 (February 15, 2021): 1921. http://dx.doi.org/10.3390/ijms22041921.
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Solid organ transplantation is a gold standard treatment for patients suffering from an end-stage organ disease. Patient and graft survival have vastly improved during the last couple of decades; however, the field of transplantation still encounters several unique challenges, such as a shortage of transplantable organs and increasing pool of extended criteria donor (ECD) organs, which are extremely prone to ischemia-reperfusion injury (IRI), risk of graft rejection and challenges in immune regulation. Moreover, accurate and specific biomarkers, which can timely predict allograft dysfunction and/or rejection, are lacking. The essential amino acid tryptophan and, especially, its metabolites via the kynurenine pathway has been widely studied as a contributor and a therapeutic target in various diseases, such as neuropsychiatric, autoimmune disorders, allergies, infections and malignancies. The tryptophan-kynurenine pathway has also gained interest in solid organ transplantation and a variety of experimental studies investigating its role both in IRI and immune regulation after allograft implantation was first published. In this review, the current evidence regarding the role of tryptophan and its metabolites in solid organ transplantation is presented, giving insights into molecular mechanisms and into therapeutic and diagnostic/prognostic possibilities.
Dissertations / Theses on the topic "Graft rejection; Tumours; Autoimmune diseases"
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Chinaelli, Marco. "99mTc labelling of interleukin-2 for in-vivo detection of lymphocytic infiltration." Thesis, Queen Mary, University of London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.243365.
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Lambert, Julie. "Autoimmune Diabetes and Transplantation Tolerance Induced by Costimulation Blockade in NOD Mice: a Dissertation." eScholarship@UMMS, 2007. https://escholarship.umassmed.edu/gsbs_diss/344.
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NOD mice model human type 1 diabetes and have been used to investigate tolerance induction protocols for islet transplantation in a setting of autoimmunity. Costimulation blockade-based tolerance protocols that induce prolonged skin and permanent islet allograft survival in non-autoimmune mice have failed in NOD mice. To investigate the underlying mechanisms, we generated NOD hematopoietic chimeras. We were able to show that dendritic cell maturation defects seen in NOD mice are partially corrected in mixed hematopoietic chimeras. Furthermore, skin allograft survival was dependent upon the phenotype of the bone marrow donor, demonstrating that in the NOD the resistance to tolerance induction resides in the hematopoietic compartment. In addition, we studied congenic NOD mice bearing insulin dependent diabetes (Idd) loci that reduce diabetes incidence. The incidence of diabetes is reduced in NOD.B6 Idd3 mice, and virtually absent in NOD.B6 Idd3Idd5 mice. Islet allograft survival in NOD.B6 Idd3 mice is prolonged as compared to NOD mice, and in NOD.B6 Idd3Idd5 mice islet allograft survival is similar to that achieved in C57BL/6 mice. Alloreactive CD8 T cell depletion in NOD mice treated with costimulation blockade is impaired, but is partially restored in NOD.B6 Idd3 mice, and completely restored in NOD.B6 Idd3Idd5 mice. Idd3 results from variations in Il2 gene transcription. We hypothesized insufficient levels of IL-2 in NOD mice contributes to impaired deletion of alloreactive CD8 T cells and shortened islet allograft survival. We observed using synchimeric mice that co-administration of exogenous IL-2 to NOD mice treated with costimulation blockade led to deletion of alloreactive CD8 T cells comparable to that in C57BL/6 mice and prolonged islet allograft survival. However, some Idd loci impaired the induction of transplantation tolerance. These data suggest that Idd loci can facilitate or impair induction of transplantation tolerance by costimulation blockade, and that Idd3 (IL-2) is critical component in this process.
Book chapters on the topic "Graft rejection; Tumours; Autoimmune diseases"
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Nocentini, Giuseppe, Luigi Cari, Graziella Migliorati, and Carlo Riccardi. "Treatment of Autoimmune Diseases and Prevention of Transplant Rejection and Graft-Versus-Host Disease by Regulatory T Cells: The State of the Art and Perspectives." In The Epigenetics of Autoimmunity, 321–57. Elsevier, 2018. http://dx.doi.org/10.1016/b978-0-12-809912-4.00016-7.
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