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Добірка наукової літератури з теми "MSC, GvHD, IMMUNOTHERAPY"

Автор: Grafiati

Опубліковано: 11 березня 2023

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Статті в журналах з теми "MSC, GvHD, IMMUNOTHERAPY"

Lim, Jisun, Jinbeom Heo, Hyein Ju, Ji-Woong Shin, YongHwan Kim, Seungun Lee, Hwan Yeul Yu, et al. "Glutathione dynamics determine the therapeutic efficacy of mesenchymal stem cells for graft-versus-host disease via CREB1-NRF2 pathway." Science Advances 6, no. 16 (April 2020): eaba1334. http://dx.doi.org/10.1126/sciadv.aba1334.

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Анотація:

Glutathione (GSH), the most abundant nonprotein thiol functioning as an antioxidant, plays critical roles in maintaining the core functions of mesenchymal stem cells (MSCs), which are used as a cellular immunotherapy for graft-versus-host disease (GVHD). However, the role of GSH dynamics in MSCs remains elusive. Genome-wide gene expression profiling and high-throughput live-cell imaging assays revealed that CREB1 enforced the GSH-recovering capacity (GRC) of MSCs through NRF2 by directly up-regulating NRF2 target genes responsible for GSH synthesis and redox cycling. MSCs with enhanced GSH levels and GRC mediated by CREB1-NRF2 have improved self-renewal, migratory, anti-inflammatory, and T cell suppression capacities. Administration of MSCs overexpressing CREB1-NRF2 target genes alleviated GVHD in a humanized mouse model, resulting in improved survival, decreased weight loss, and reduced histopathologic damages in GVHD target organs. Collectively, these findings demonstrate the molecular and functional importance of the CREB1-NRF2 pathway in maintaining MSC GSH dynamics, determining therapeutic outcomes for GVHD treatment.

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Karlsson, Helen, Sujith Samarasinghe, Lynne M. Ball, Berit Sundberg, Arjan C. Lankester, Francesco Dazzi, Mehmet Uzunel, et al. "Mesenchymal stem cells exert differential effects on alloantigen and virus-specific T-cell responses." Blood 112, no. 3 (August 1, 2008): 532–41. http://dx.doi.org/10.1182/blood-2007-10-119370.

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Abstract Mesenchymal stem cells (MSCs) suppress alloantigen-induced T-cell functions in vitro and infusion of third-party MSCs seems to be a promising therapy for graft-versus-host disease (GVHD). Little is known about the specificity of immunosuppression by MSCs, in particular the effect on immunity to pathogens. We have studied how MSCs affect T-cell responses specific to Epstein-Barr virus (EBV) and cytomegalovirus (CMV). We found that EBV- and CMV-induced proliferation and interferon-γ (IFN-γ) production from peripheral blood mononuclear cells (PBMCs) was less affected by third-party MSCs than the response to alloantigen and that MSCs had no effect on expansion of EBV and CMV pentamer-specific T cells. Established EBV-specific cytotoxic T cells (CTL) or CMV-CTL cultured with MSCs retained the ability to proliferate and produce IFN-γ in response to their cognate antigen and to kill virally infected targets. Finally, PBMCs from 2 patients who received MSCs for acute GVHD showed persistence of CMV-specific T cells and retained IFN-γ response to CMV after MSC infusion. In summary, MSCs have little effect on T-cell responses to EBV and CMV, which contrasts to their strong immunosuppressive effects on alloreactive T cells. These data have major implications for immunotherapy of GVHD with MSCs and suggest that the effector functions of virus-specific T cells may be retained after MSC infusion.

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Sangiorgi, Bruno, and Rodrigo Alexandre Panepucci. "Modulation of Immunoregulatory Properties of Mesenchymal Stromal Cells by Toll-Like Receptors: Potential Applications on GVHD." Stem Cells International 2016 (2016): 1–10. http://dx.doi.org/10.1155/2016/9434250.

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Анотація:

In the last decade, the immunomodulatory properties of mesenchymal stromal cells (MSCs) have attracted a lot of attention, due to their potential applicability in the treatment of graft-versus-host disease (GVHD), a condition frequently associated with opportunistic infections. The present review addresses how Pathogen-Associated Molecular Patterns (PAMPS) modulate the immunosuppressive phenotype of human MSCs by signaling through Toll-like receptors (TLRs). Overall, we observed that regardless of the source tissue, human MSCs express TLR2, TLR3, TLR4, and TLR9. Stimulation of distinct TLRs on MSCs elicits distinct inflammatory signaling pathways, differentially influencing the expression of inflammatory factors and the ability of MSCs to suppress the proliferation of immune system cells. The capacity to enhance the immunosuppressive phenotype of MSCs through TLRs stimulation might be properly elucidated in order to improve the MSC-based immunotherapy against GVHD.

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Boni, Andrea, Pawel Muranski, Claudia Wrzesinski, Andrew Kaiser, Chrystal Paulos, Douglas Palmer, Luca Gattinoni, and Nicholas P. Restifo. "Partly MHC Matched Allogeneic Tumor Specific T Cells Mediate Tumor Regression without Inducing GVHD in Immunosuppressed Host." Blood 108, no. 11 (November 16, 2006): 5210. http://dx.doi.org/10.1182/blood.v108.11.5210.5210.

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Abstract Adoptive cell transfer (ACT) immunotherapy following lymphodepleting conditioning is a promising strategy for the treatment of metastatic solid tumors, however the difficulties in generating autologous tumor specific lymphocytes for every patient has significantly limited its applications. Allogeneic partly matched tumor specific T cells could be used for patients in whom autologous cells are not available, however their rapid rejection by the host restricts this approach. When CD8+ pmel-1 T cells from B6-BALB-C F1 (b/d) were transferred into B16 tumor-bearing B6 mice (b/b) or into a different F1 (b/k), these tumor-specific T cells were rapidly rejected, and had no impact on the tumor regression. Here we show that following myeloablative conditioning, the adoptive transfer of allogeneic, major histocompatibility mismatched tumor-specific T lymphocytes resulted in the regression of large vascularized tumors. The ability of adoptively transferred allogeneic T cells to mediate tumor regression was directly proportional to the dose of irradiation given prior T cell transfer which also correlated with the in vivo survival of the transferred cells. At the highest irradiation dose used (i.e. 11 Gy) allogeneic T cells could survive for as long as 4 weeks and their efficacy was comparable to syngeneic tumor-reactive T cells. In addition we found that the risk of inducing a graft versus host (GVH) reaction was minor when the specificity of transferred TCR is confined. In fact co-transfer of transgenic cells and small amounts of open repertoire T cells (2*10e4) able to react with the host did not result in any measurable toxicity whereas co transfer of greater quantities (2*10e5 or more) could cause fatal GVHD effect. Interestingly GVH reaction was associated with an improved tumor treatment, though this effect was transient as most of the animals succumbed to GVHD. Here we demonstrate that allogeneic T cells might represent an important tool in cancer immunotherapy allowing treatment of patients for whom it is not possible to obtain autologous cells. Furthermore the possible synergy between tumor specific allogeneic T cells and GVH effect could be exploited in bone marrow transplant protocols.

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Fang, Ying, Yichen Zhu, Adam Kramer, Yuning Chen, Yan-Ruide Li, and Lili Yang. "Graft-versus-Host Disease Modulation by Innate T Cells." International Journal of Molecular Sciences 24, no. 4 (February 17, 2023): 4084. http://dx.doi.org/10.3390/ijms24044084.

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Анотація:

Allogeneic cell therapies, defined by genetically mismatched transplantation, have the potential to become a cost-effective solution for cell-based cancer immunotherapy. However, this type of therapy is often accompanied by the development of graft-versus-host disease (GvHD), induced by the mismatched major histocompatibility complex (MHC) between healthy donors and recipients, leading to severe complications and death. To address this issue and increase the potential for allogeneic cell therapies in clinical practice, minimizing GvHD is a crucial challenge. Innate T cells, encompassing subsets of T lymphocytes including mucosal-associated invariant T (MAIT) cells, invariant natural killer T (iNKT) cells, and gamma delta T (γδ T) cells, offer a promising solution. These cells express MHC-independent T-cell receptors (TCRs), allowing them to avoid MHC recognition and thus GvHD. This review examines the biology of these three innate T-cell populations, evaluates research on their roles in GvHD modulation and allogeneic stem cell transplantation (allo HSCT), and explores the potential futures for these therapies.

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Kwiatkowska-Borowczyk, Eliza P., Anna Kozłowska, Klaudia Maruszak, Luiza Kańczuga-Koda, Mariusz Koda, Monika Dajnowiec, Andrzej Mackiewicz, and Dariusz W. Kowalczyk. "Adoptive transfer of tumor specific T cells from allogeneic donors is feasible, effective and safe alternative to autologous T cell based tumor immunotherapy." Journal of Medical Science 83, no. 1 (March 30, 2014): 21–28. http://dx.doi.org/10.20883/medical.e39.

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Donor lymphocyte infusion is used to increase the graft versus tumor (GVT) effect after allogeneic hematopoietic cell transplant. The limited spectrum of activity and high risk of graft versus host disease (GVHD) remain major limitations of this approach. The finding of new cell populations for adoptive immunotherapy, with the ability to separate GVT from GVHD, would be useful. In the present manuscript, we tested in mouse model the use of allogeneic MHC partially matched effector cells for adoptive T cell immunotherapy of cancer. We sought to maximize graft-versus-tumor effect while minimizing GVHD using tumor-specific allogeneic effector T cells rather than open-repertoire T cells. A F1 hybrid (Balb/c x C57BL/6) -MethA-EGFP–bearing mice received a preparative regimen of nonmyeloablating cyclophosphamide lymphodepletion followed by adoptive transfer of bulk Balb/c derived allogeneic T cells specific for the MethA-EGFP tumor cells. Adoptively transferred allogeneic tumor-specific T lymphocytes prevented tumor formation without graft versus host disease – like symptoms. We found that the risk of GVHD was low even with high number of transferred tumor-specific T cells. These data indicate that the use of tumor-specific allogeneic T cells is feasible, effective and safe alternative to autologous T cell based tumor immunotherapy.

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Marcus, Assaf, Tova Waks, and Zelig Eshhar. "Tumor immunotherapy using chimeric receptor redirected allogeneic T cells across MHC barriers (131.39)." Journal of Immunology 184, no. 1_Supplement (April 1, 2010): 131.39. http://dx.doi.org/10.4049/jimmunol.184.supp.131.39.

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Анотація:

Abstract We present a strategy for adoptive immunotherapy using fully mismatched allogeneic chimeric receptor redirected T cells (allo-'T-bodies') in the absence of Graft vs. Host disease (GvHD). The strategy hinges on creating a therapeutic time-window using mild preconditioning which on one hand allows the allogeneic T-bodies enough time to effectively attack the tumor but on the other hand does not ablate the Host vs. Graft response (HvG) ensuring the eventual rejection of the allogeneic T cells thus preventing GvHD. We found that transfer of fully mismatched allogeneic T cells expressing a HER2/neu specific chimeric receptor following mild preconditioning roughly tripled the median survival of mice bearing pulmonary Renca-HER2 metastases with around 50% of mice surviving long term (>200 days) in the absence of GvHD mortality. We show that allo-T-bodies provide comparable benefit to syngeneic T-bodies, and are far superior to non-specific allogeneic T cells, demonstrating that the response is indeed tumor-specific and not merely allo-specific. Taken together these data provide proof of principle for safe and effective allogeneic adoptive therapy allowing for the use of 'universal effector cells' as a standardized treatment for cancer.

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Luznik, Leo, Sanju Jalla, Laura W. Engstrom, Robert Iannone, and Ephraim J. Fuchs. "Durable engraftment of major histocompatibility complex–incompatible cells after nonmyeloablative conditioning with fludarabine, low-dose total body irradiation, and posttransplantation cyclophosphamide." Blood 98, no. 12 (December 1, 2001): 3456–64. http://dx.doi.org/10.1182/blood.v98.12.3456.

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Abstract Treatment of leukemia by myeloablative conditioning and transplantation of major histocompatibility complex (MHC)–mismatched stem cells is generally avoided because of the high risk of graft rejection or lethal graft-versus-host disease (GVHD). This study shows that MHC-incompatible cells can engraft stably after nonmyeloablative conditioning with immunosuppressive chemotherapy and low-dose total body irradiation (TBI). Long-term mixed hematopoietic chimerism, clonal deletion of donor-reactive T cells, and bidirectional cytotoxic T-cell tolerance were achieved by transplanting MHC-mismatched marrow cells into recipients conditioned with pretransplantation fludarabine or cyclophosphamide (Cy), 50 to 200 cGy TBI on day −1, and Cy 200 mg/kg intraperitoneally on day 3. In this model, long-term donor chimerism was proportional to the dose of TBI or donor marrow cells. Pretransplantation fludarabine and posttransplantation Cy were both required for alloengraftment, but the drugs had additional effects. For example, fludarabine sensitized host stem cells to the toxicity of TBI, because animals conditioned with both agents had higher chimerism than animals conditioned with TBI alone (P < .05). Also, posttransplantation Cy attenuated lethal and nonlethal GVH reactions, because F1 recipients of host-reactive, parental spleen cells survived longer (P < .05) and had lower donor cell chimerism (P < .01) if they received posttransplantation Cy than if they did not. Finally, delayed infusions of donor lymphocytes into mixed chimeras prolonged survival after leukemia challenge (P < .0001) without causing lethal GVHD. These results indicate that stable engraftment of MHC-incompatible cells can be induced after fludarabine-based, nonmyeloablative conditioning and that it serves as a platform for adoptive immunotherapy with donor lymphocyte infusions.

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Waller, Edmund K., Alan M. Ship, Stephen Mittelstaedt, Timothy W. Murray, Richard Carter, Irina Kakhniashvili, Sagar Lonial, Jeannine T. Holden, and Michael W. Boyer. "Irradiated Donor Leukocytes Promote Engraftment of Allogeneic Bone Marrow in Major Histocompatibility Complex Mismatched Recipients Without Causing Graft-Versus-Host Disease." Blood 94, no. 9 (November 1, 1999): 3222–33. http://dx.doi.org/10.1182/blood.v94.9.3222.

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Abstract Graft rejection in allogeneic bone marrow transplantation (BMT) can occur when donor and recipient are mismatched at one or more major histocompatibility complex (MHC) loci. Donor T cells can prevent graft rejection, but may cause fatal graft-versus-host disease (GVHD). We tested whether irradiation of allogeneic donor lymphocytes would preserve their graft-facilitating activity while inhibiting their potential for GVHD. Infusions of irradiated allogeneic T cells did not cause GVHD in MHC-mismatched SJL → (SJL × C57BL6) F1, C57BL6 → B10.RIII, and C57BL6 → B10.BR mouse donor → recipient BMT pairs. The 60-day survival among MHC-mismatched transplant recipients increased from 2% (BM alone) to up to 75% among recipients of BM plus irradiated allogeneic splenocytes. Optimal results were obtained using 50 × 106 to 75 × 106 irradiated donor splenocytes administered in multiple injections from day −1 to day +1. Recipients of an equal number of nonirradiated MHC-mismatched donor splenocytes uniformly died of acute GVHD. The graft facilitating activity of the irradiated allogeneic splenocytes was mediated by donor T cells. Irradiation to 7.5 Gy increased nuclear NFκB in T cells and their allospecific cytotoxicity. Irradiated T cells survived up to 3 days in the BM of MHC-mismatched recipients without proliferation. Recipients of irradiated allogeneic splenocytes and allogeneic BM had stable donor-derived hematopoiesis without a significant representation of donor splenocytes in the T-cell compartment. Irradiated allogeneic T cells thus represent a form of cellular immunotherapy with time-limited biologic activity in vivo that can facilitate allogeneic BMT without causing GVHD.

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Анотація:

Graft rejection in allogeneic bone marrow transplantation (BMT) can occur when donor and recipient are mismatched at one or more major histocompatibility complex (MHC) loci. Donor T cells can prevent graft rejection, but may cause fatal graft-versus-host disease (GVHD). We tested whether irradiation of allogeneic donor lymphocytes would preserve their graft-facilitating activity while inhibiting their potential for GVHD. Infusions of irradiated allogeneic T cells did not cause GVHD in MHC-mismatched SJL → (SJL × C57BL6) F1, C57BL6 → B10.RIII, and C57BL6 → B10.BR mouse donor → recipient BMT pairs. The 60-day survival among MHC-mismatched transplant recipients increased from 2% (BM alone) to up to 75% among recipients of BM plus irradiated allogeneic splenocytes. Optimal results were obtained using 50 × 106 to 75 × 106 irradiated donor splenocytes administered in multiple injections from day −1 to day +1. Recipients of an equal number of nonirradiated MHC-mismatched donor splenocytes uniformly died of acute GVHD. The graft facilitating activity of the irradiated allogeneic splenocytes was mediated by donor T cells. Irradiation to 7.5 Gy increased nuclear NFκB in T cells and their allospecific cytotoxicity. Irradiated T cells survived up to 3 days in the BM of MHC-mismatched recipients without proliferation. Recipients of irradiated allogeneic splenocytes and allogeneic BM had stable donor-derived hematopoiesis without a significant representation of donor splenocytes in the T-cell compartment. Irradiated allogeneic T cells thus represent a form of cellular immunotherapy with time-limited biologic activity in vivo that can facilitate allogeneic BMT without causing GVHD.

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Дисертації з теми "MSC, GvHD, IMMUNOTHERAPY"

Alessandro, Gatti. "Isolation, expansion and functional characterization of hPL-expanded hBM-MSC for the treatment of systemic and severe acute Graft-versus-Host Disease." Doctoral thesis, 2018. http://hdl.handle.net/11562/978782.

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In this study, we first developed an expansion protocol for human bone marrow derived-MSC (hBM-MSC) using two different supplements for culture media, i.e. fetal bovine serum (FBS) or human platelet lysate (hPL). Interestingly, hPL supplement was more effective than FBS in expanding MSC. Afterwards, we characterized MSC and confirmed their genome stability through karyotype analysis and real time-PCR. MSC were then assessed in vitro for their ability to acquire the anti-inflammatory phenotype necessary for avoiding immune rejection and modulating host immune effector cells. MSC priming with TNF-α and IFN-γ led to increased ability in preventing NK cell-mediated lysis. Moreover, using standardized proliferation assays, MSC displayed strong immune suppressive activity towards T, B and NK cells. We then obtained a reproducible xenogeneic mouse model of aGvHD that was used to assess in vivo the efficacy of hPL-expanded MSC-based immunotherapy with different schedules of MSC administration

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