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Academic literature on the topic 'GvL and GvHD'

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Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "GvL and GvHD"

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Litvinova, Elena, Sébastien Maury, Olivier Boyer, Sylvie Bruel, Laurent Benard, Gilbert Boisserie, David Klatzmann, and José L. Cohen. "Graft-versus-leukemia effect after suicide-gene–mediated control of graft-versus-host disease." Blood 100, no. 6 (September 15, 2002): 2020–25. http://dx.doi.org/10.1182/blood-2002-01-0161.

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Abstract Clinical data indicate that after allogeneic hematopoietic stem cell transplantation (HSCT) for hematological malignancies, the graft-versus-leukemia (GVL) effect is in large part mediated by the graft-versus-host reaction (GVHR), which also often leads to graft-versus-host disease (GVHD). Controlling alloreactivity to prevent GVHD while retaining GVL poses a true dilemma for the successful treatment of such malignancies. We reasoned that suicide gene therapy, which kills dividing cells expressing the thymidine kinase (TK) “suicide” gene using time-controlled administration of ganciclovir (GCV), might solve this dilemma. We have previously shown that after infusion of allogeneic TK T cells along with HSCT to an irradiated recipient, an early and short GCV treatment efficiently prevents GVHD by selectively eliminating alloreactive T cells while sparing nonalloreactive T cells, which can then contribute to immune reconstitution. Nevertheless, it remained to be established that this therapeutic strategy retained the desired GVL effect. Hypothesizing that a contained GVHR would be essential, we evaluated the GVL effect using different protocols of GCV administration. We were able to show that when the GCV treatment is initiated at, or close to, the time of grafting, GVHD is controlled but GVL is lost. In contrast, when the onset of GCV administration is delayed until day 6, a potent GVL effect is retained while GVHD is still controlled. These data emphasize that, by a time-optimized scheduling of the administration of GCV, this TK/GCV strategy can be tuned to efficiently treat malignant hemopathies.
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Johnson, B. D., C. McCabe, C. A. Hanke, and R. L. Truitt. "Use of anti-CD3 epsilon F(ab')2 fragments in vivo to modulate graft-versus-host disease without loss of graft-versus-leukemia reactivity after MHC-matched bone marrow transplantation." Journal of Immunology 154, no. 10 (May 15, 1995): 5542–54. http://dx.doi.org/10.4049/jimmunol.154.10.5542.

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Abstract The use of T cell-specific mAb in vivo for prevention and treatment of graft-vs-host disease (GVHD) and its impact on graft-vs-leukemia (GVL) reactivity was examined in a murine model of MHC-matched bone marrow transplantation (BMT). F(ab')2 fragments of a CD3 epsilon-specific mAb were administered to irradiated AKR (H-2k) hosts after transplantation of BM plus spleen cells from B10.BR donors (BMS chimeras). The effects on GVH and GVL reactivity were Ab dose- and schedule-dependent. A short course of mAb (qe2d, days 0 to 8) prevented clinical evidence of GVHD and mortality. Anti-CD3 F(ab')2 mAb reversed clinical symptoms of acute GVHD when delayed up to 18 days post-transplant. Anti-host (Mls-1a)-specific V beta 6+ cells were absent from the spleens of GVH-negative control mice, but persisted in Ab-treated BMS chimeras despite the absence of GVHD. Leukemic mice given 16.7 micrograms of Ab on days 0, 2, and 4 survived leukemia-free without developing severe GVHD. A longer course of Ab completely prevented GVHD, but led to leukemia relapse in tumor-bearing hosts, despite engraftment of donor T cells. The GVL effect was quantitatively stronger when Ab was used for GVH therapy as compared with GVH prevention. Some Ab-treated, GVH-free chimeras relapsed with lymphomas in unusual sites, suggesting that occult tumor cells may persist in nonlymphoid tissues. These experiments demonstrate that T cell-specific mAb can be used successfully in vivo to avoid severe GVHD, but that excessive or ill-timed administration of Ab may eliminate GVL reactivity.
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Jadi, Othmane, Hancong Tang, Junke Wang, Dante Bortone, Steven Vensko, Loreall Pooler, Xin Sheng, et al. "Associations of Clinical Outcomes after Allogeneic Hematopoietic Cell Transplantation with Number of Predicted Class II Restricted mHA." Blood 136, Supplement 1 (November 5, 2020): 2. http://dx.doi.org/10.1182/blood-2020-142017.

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Background: Leukemia relapse after allogeneic hematopoietic cell transplantation (alloHCT) has been associated with loss of heterozygosity of class II HLA, suggesting that T cells targeting leukemia via class II interactions may be critical for graft-vs-leukemia (GvL) effects and protection from relapse (Zeiser & Vago, 2019). Therefore, we aimed to determine whether the number of predicted class-II restricted minor histocompatibility antigens (mHAs) in alloHCT recipients associates with clinical outcome. Specifically, we investigated: (1) if the number of mHAs expressed on leukemia and bone marrow cells (GvL mHAs) is correlated with incidence of leukemia relapse, and/or (2) if mHAs expressed on acute graft versus host disease (GvHD) target organs (GvH mHAs) correlated with incidence of GvHD. We expected increased GvL mHAs to be associated with increased survival, and increased GvH mHAs to be associated with increased incidence of GvHD. Methods: The study population was derived from donor-recipient alloHCT pairs (DRPs) treated for Acute Myeloid Leukemia (AML), Acute Lymphocytic Leukemia (ALL), and Myelodysplastic Syndrome (MDS) from the CIBMTR and previously analyzed in DISCOVeRY-BMT. To predict HLA class II restricted mHAs in alloHCT recipients, we translated nonsynonymous single nucleotide variants present in each recipient, but absent in their respective donor, into all possible peptides 15-24 amino acids long. We used netMHCIIpan to score these peptides and select those most likely to be presented (Reynisson et al., 2020). Predicted mHAs highly expressed in skin, hepatobiliary, and bowel tissues were classified as GvH mHAs, and those highly expressed highly in, testis, and bone marrow were classified as GvL mHAs. The impact of mHA on disease related mortality (DRM), leukemia free survival (LFS), disease relapse and death due to GVHD were assessed with competing risk models. We next determined whether knowledge of the number of GvL and GvH mHAs improves the ability of models to predict clinical outcome. We fit optimal logistic regression models (elastic net regularization with Monte Carlo cross validation) to predict GvHD mortality and relapse mortality at 1 year after alloHCT using: (1) clinical data only, and (2) both clinical data and number of GvH/GvL mHAs. Lastly, using the same regularization and cross-validation procedures as above, we determined which variables contributed most to the Cox regression models of overall survival. Results: The number of GvL-restricted and GvH-restricted class-II mHAs were significantly correlated (Figure 1). Patients who died of disease before 1 year after alloHCT had significantly fewer GvL mHAs when controlling for covariates (HR=.89, 95% CI .89, .99, P= 0.04) (Figure 2). There was no association between GvL mHAs and LFS or relapse. Surprisingly, death due to GvHD by 1 year after alloHCT was lower for recipients with more GvL mHAs (HR=.88, 95% CI= .76, 1.01 , P=.08) (Figure 3), however, because GvH and GvL mHAs are highly correlated, we believe this reflects better overall survival associated with increased GvL mHAs. Neither the predictive models that included the number of GvH/GvL mHAs nor the Cox regression models fitted with GvL mHA numbers performed better than models trained on clinical data alone (Figure 4). Conclusions: GvL mHAs were inversely associated with DRM at 1-year post-alloHCT as expected. Contrary to our hypothesis, the number of GvH mHAs was inversely associated with GvHD mortality at 1 year. This may reflect better overall survival associated with increased GvL mHAs, as GvH and GvL mHAs are highly correlated. The potential association between class-II mHAs and DRM warrant further investigation and validation. If validated, this supports the development of class-II mHA targeted immunotherapies. Disclosures Pasquini: Bristol Myers Squibb: Consultancy; BMS: Membership on an entity's Board of Directors or advisory committees, Research Funding; Amgen: Other; Novartis: Research Funding; Kite: Research Funding. Armistead:GeneCentric: Consultancy; Cell Microsystems: Patents & Royalties: Patent application U.S. 16/347,104 "Automated collection of a specified number of cells". Vincent:GeneCentric Therapeutics: Consultancy.
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Das, Rupali, Richard Komorowski, Martin J. Hessner, Hariharan Subramanian, Claudia S. Huettner, Daniel Cua, and William R. Drobyski. "Blockade of interleukin-23 signaling results in targeted protection of the colon and allows for separation of graft-versus-host and graft-versus-leukemia responses." Blood 115, no. 25 (June 24, 2010): 5249–58. http://dx.doi.org/10.1182/blood-2009-11-255422.

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Abstract Allogeneic stem cell transplantation is the most potent form of effective adoptive immunotherapy. The graft-versus-leukemia (GVL) effect mediated by the allogeneic graft, however, is typically coexpressed with graft-versus-host disease (GVHD), which is the major complication of allogeneic stem cell transplantation. In this study, we used genetic and antibody-based strategies to examine the effect that blockade of interleukin 23 (IL-23) signaling had on GVH and GVL reactivity in murine transplantation recipients. These studies demonstrate that the selective protection of the colon that occurs as a consequence of inhibition of IL-23 signaling reduces GVHD without loss of the GVL effect. The separation of GVH and GVL reactivity was noted in both acute and chronic hematologic malignancy models, indicating that this approach was not restricted by the kinetic profile of the underlying leukemia. Furthermore, a potent GVL response could be mounted in the colon under conditions where tumor cells migrated to this site, indicating that this organ did not serve as a sanctuary site for subsequent systemic relapse in GVHD-protected animals. These studies demonstrate that blockade of IL-23 signaling is an effective strategy for separating GVH and GVL responses and identify IL-23 as a therapeutic target for the regulation of alloresponses in humans.
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Lehmann, Percy. "Stärken der Graft-versus-Leukämie-Effekte durch richtig terminierte Photochemotherapie." Kompass Dermatologie 6, no. 3 (2018): 149–50. http://dx.doi.org/10.1159/000489283.

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Background: Cure of acute leukemia after transplantation is mediated by the grafted cells. We investigated the graft-versus-leukemia effect (GVL) in patients with cutaneous acute graft-versus-host disease (GVHD) treated with photochemotherapy (psoralen and ultraviolet light type A). Method: Forty-seven patients with acute leukemia were followed 5,000 days after transplantation to assess survival and GVL by multivariate analysis. The primary predictor was time to treatment of cutaneous acute GVHD by photochemotherapy separated into treatment start during the first week of acute GVHD versus after the first week of acute GVHD. Results: Photochemotherapy started after the first week of acute GVHD predicted GVL with a hazard ratio (HR) of 3.94 (95% confidence interval, CI, 1.67-9.33, p = 0.0018) and survival with preserved GVL with an HR of 2.63 (95% CI 1.30-5.32, p = 0.007). The effects on GVL and survival with preserved GVL were present regardless of whether the patients were transplanted in remission or relapse (p < 0.05). Chronic GVHD came earlier in the group that started photochemotherapy after 1 week of acute GHVD, but chronic GVHD did not increase the GVL. Conclusion: The timing of photochemotherapy after cutaneous acute GVHD may direct the GVL and predict long-term leukemia-free survival.
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Matte-Martone, Catherine, Jinli Liu, Dhanpat Jain, Jennifer McNiff, and Warren D. Shlomchik. "CD8+ but not CD4+ T cells require cognate interactions with target tissues to mediate GVHD across only minor H antigens, whereas both CD4+ and CD8+ T cells require direct leukemic contact to mediate GVL." Blood 111, no. 7 (April 1, 2008): 3884–92. http://dx.doi.org/10.1182/blood-2007-11-125294.

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Abstract Whether T-cell antigen receptors (TCR) on donor T cells require direct interactions with major histocompatibility complex class I or class II (MHCI/MHCII) molecules on target cells to mediate graft-versus-host disease (GVHD) and graft-versus-leukemia (GVL) is a fundamental question in allogeneic stem-cell transplantation (alloSCT). In MHC-mismatched mouse models, these contacts were not required for GVHD. However, this conclusion may not apply to MHC-matched, multiple minor histocompatibility antigen-mismatched alloSCT, the most common type performed clinically. To address this, we used wild-type (wt)→MHCI−/− or wt→MHCII−/− bone marrow chimeras as recipients in GVHD experiments. For GVL experiments, we used MHCI−/− or MHCII−/− chronic-phase CML cells created by expressing the BCR-ABL cDNA in bone marrow from MHCI−/− or MHCII−/− mice. TCR/MHCI contact was obligatory for both CD8-mediated GVHD and GVL. In contrast, CD4 cells induced GVHD in wt→MHCII−/− chimeras, whereas MHCII−/− mCP-CML was GVL-resistant. Donor CD4 cells infiltrated affected skin and bowel in wt→MHCII−/− recipients, indicating that they mediated GVHD by acting locally. Thus, CD4 cells use distinct effector mechanisms in GVHD and GVL: direct cytolytic action is required for GVL but not for GVHD. If these noncytolytic pathways can be inhibited, then GVHD might be ameliorated while preserving GVL.
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Heinrichs, Jessica Lauren, Hung Nguyen, David Bastian, Yongxia Wu, Anusara Daenthanasanmak, and Xue-Zhong Yu. "CD8 Tregs Promote Gvhd Prevention and Restore Impaired GVL Effect Mediated By CD4 Tregs in Mice." Blood 126, no. 23 (December 3, 2015): 1873. http://dx.doi.org/10.1182/blood.v126.23.1873.1873.

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Abstract Adoptive regulatory T-cell (Treg) therapy has enhanced the outcome of patients suffering from graft-versus-host (GVH) disease following allogeneic hematopoietic stem cell transplantation (allo-HCT); however, fear of broad immune suppression and subsequent dampening of the beneficial graft-versus-leukemic (GVL) responses remains a challenge. In order to subvert broad immune suppression, we generated alloantigen-specific induced Tregs (iTregs) from resting CD4 or CD8 T cells and tested the ability of iTregs to suppress GVH and maintain GVL responses. We utilized a clinically relevant murine model of haploidentical-HCT with the addition of host-original leukemia cell line to evaluate the effects of CD4 and CD8 iTregs in GVH and GVL responses. While alloantigen-specific CD4 iTregs were effective in preventing GVHD (Fig. 1 A and C), they completely abrogated the GVL effect against aggressive leukemia resulting in 100% tumor mortality (Fig. 1 B and D). Mechanistically, these CD4 iTregs were found to potently suppress the expansion of effector T cells (Teffs) and their ability to secrete IFNγ and granzyme B in the recipient spleen and liver, which may contribute to the impaired GVL activity. Using similar approach, we generated alloantigen-specific CD8 iTregs and found they express higher levels of granzyme B and CTLA-4 compared to nTreg and CD4 iTregs. In vivo studies showed these CD8 iTregs moderately attenuated GVHD (Fig. 1 A and C)while completely sparing the GVL effect (Fig. 1 B and D). We thus further reasoned that the combination of CD4 and CD8 iTregs could achieve the optimal goal of allo-HCT: GVHD suppression with GVL preservation. Indeed, the combination therapy potently suppressed GVHD resulting in increased survival and decreased pathological injury to target organs than either CD4 or CD8 iTreg singular therapy (Fig. 1 A and C). More importantly, the combination therapy maintained potent GVL responses reflected by significantly decreased tumor mortality and load (Fig. 1 B and D).Mechanistically, we observed addition of CD8 iTregs maintained the suppression of Teff expansion but restored the ability of Teffs in producing inflammatory cytokines (e.g. IFNγ and TFNα) and cytolytic effector molecules (e.g. granzyme B and TRAIL). To our knowledge the current findings are the first to support the use of combinational iTreg therapy to achieve optimal suppression of GVHD while maintaining GVL responses. This work was supported by NIH grants: R01 CA118116 and R01 CA169116 Disclosures No relevant conflicts of interest to declare.
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Hess, Allan D. "Separation of GVHD and GVL." Blood 115, no. 9 (March 4, 2010): 1666–67. http://dx.doi.org/10.1182/blood-2009-11-254946.

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Li, Jian-Ming, Cynthia R. Giver, Ying Lu, Mohammad S. Hossain, Mojtaba Akhtari, and Edmund K. Waller. "Separating graft-versus-leukemia from graft-versus-host disease in allogeneic hematopoietic stem cell transplantation." Immunotherapy 1, no. 4 (July 2009): 599–621. http://dx.doi.org/10.2217/imt.09.32.

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Routine methods to maximize the graft-versus-leukemia (GvL) activity of allogeneic hematopoietic stem cell transplantation (HSCT) without the detrimental effects of graft-versus-host disease (GvHD) are lacking. Depletion or inhibition of alloreactive T cells is partially effective in preventing GvHD, but usually leads to decreased GvL activity. The current model for the pathophysiology of acute GvHD describes a series of immune pathways that lead to activation of donor T cells and inflammatory cytokines responsible for tissue damage in acute GvHD. This model does not account for how allotransplant can lead to GvL effects without GvHD, or how the initial activation of donor immune cells may lead to counter-regulatory effects that limit GvHD. In this review, we will summarize new findings that support a more complex model for the initiation of GvHD and GvL activities in allogeneic HSCT, and discuss the potential of novel strategies to enhance GvL activity of the transplant.
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Fanning, Stacey, Stephanie Berger, Robert Korngold, and Thea Friedman. "Tumor-sensitized, Vβ spectratype-selected CD8+ T cells promote graft-versus-leukemia responses in the absence of severe lethal graft-versus-host disease in a murine model of allogeneic bone marrow transplantation. (145.20)." Journal of Immunology 184, no. 1_Supplement (April 1, 2010): 145.20. http://dx.doi.org/10.4049/jimmunol.184.supp.145.20.

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Abstract The successful use of allogeneic blood and marrow transplantation (BMT) in the treatment of hematological malignancies is hampered by the fact that many donor T cells responsible for mediating graft-versus-leukemia (GVL) effects are also involved in development of graft-versus-host disease (GVHD). Optimizing outcomes for allo-BMT depends upon successful separation of GVHD and GVL responses. Our work focuses on identifying host reactive and tumor reactive T cells based on TCR Vβ CDR3-size spectratype analysis. In this study, we used a MHC-matched, miHA-mismatched murine model of BMT (B10.BR→CBA) and a CBA-derived myeloid leukemia, MMC6. Previous studies have shown this GVHD model to be mediated by CD4+-independent CD8+ T cells. Here, we show that the Vβ13 family is uniquely skewed in the B10.BR anti-MMC6 CD8+ T cell response. Transplantation of CD8+Vβ13+ T cells at the dose equivalent of 10x106 CD8+ T cells, the dose at which recipient mice develop severe lethal GVHD, did not mediate GVHD or GVL. Increased doses of Vβ13+ T cells led to increased GVL responses, however, recipient mice began to exhibit symptoms of GVHD. Of most interest, when recipients were given MMC6 presensitized Vβ13+ donor T cells, they displayed a significant GVL response in the absence of lethal GVHD. These results indicate that Vβ spectratyping can be used to identify T cells uniquely skewed in GVL responses and suggest that tumor-presensitized T cells can promote GVL in the absence of GVHD.
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Dissertations / Theses on the topic "GvL and GvHD"

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Stokes, Jessica, Emely A. Hoffman, Yi Zeng, Nicolas Larmonier, and Emmanuel Katsanis. "Post-transplant bendamustine reduces GvHD while preserving GvL in experimental haploidentical bone marrow transplantation." WILEY-BLACKWELL, 2016. http://hdl.handle.net/10150/621784.

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Advances in haploidentical bone marrow transplantation (h-BMT) have drastically broadened the treatment options for patients requiring BMT. The possibility of significantly reducing the complications resulting from graft-versus-host disease (GvHD) with the administration of post-transplant cyclophosphamide (PT-CY) has substantially improved the efficacy and applicability of T cell-replete h-BMT. However, higher frequency of disease recurrence remains a major challenge in h-BMT with PT-CY. There is a critical need to identify novel strategies to prevent GvHD while sparing the graft-versus-leukaemia (GvL) effect in h-BMT. To this end, we evaluated the impact of bendamustine (BEN), given post-transplant, on GvHD and GvL using clinically relevant murine h-BMT models. We provide results indicating that post-transplant bendamustine (PT-BEN) alleviates GvHD, significantly improving survival, while preserving engraftment and GvL effects. We further document that PT-BEN can mitigate GvHD even in the absence of Treg. Our results also indicate that PT-BEN is less myelo-suppressive than PT-CY, significantly increasing the number and proportion of CD11b(+)Gr-1(hi) cells, while decreasing lymphoid cells. In vitro we observed that BEN enhances the suppressive function of myeloid-derived suppressor cells (MDSCs) while impairing the proliferation of T-and B-cells. These results advocate for the consideration of PT-BEN as a new therapeutic platform for clinical implementation in h-BMT.
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Mapara, Markus Y. "Untersuchungen im Mausmodell zu den Effekten von Spenderlymphozyteninfusionen nach allogener Knochenmaktransplantation." Doctoral thesis, [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=969434375.

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Anthony, Bryan Alan. "THE ROLE OF CD103 EXPRESSION IN PROMOTING INTESTINAL GRAFT VERSUS HOST DISEASE." The Ohio State University, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=osu1324750762.

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Cattina, Federica <1983&gt. "Studio dei polimorfismi genici degli antigeni minori di istocompatibilità e GvHD/GvL nel trapianto allogenico di cellule staminali emopoietiche." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2013. http://amsdottorato.unibo.it/5672/1/Cattina_Federica_tesi.pdf.

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L'outcome dei pazienti sottoposti a trapianto allogenico di cellule staminali emopoietiche è fortemente influenzato da graft versus leukemia (GvL) e graft versus host disease (GvHD) che sono mediate, almeno in parte, dagli antigeni minori di istocompatibilità (mHAgs). In letteratura sono stati identificati 26 mHAgs che sono stati correlati a GvHD/GvL con risultati incompleti e in alcuni casi contrastanti; inoltre manca una metodica che sia in grado di genotipizzare contemporaneamente un pannello così ampio. Il lavoro è stato finalizzato alla preparazione di un protocollo di laboratorio che permetta di studiare in modo efficace i 26 mHAgs identificati, per poi correlarli con GvHD/GvL all’interno di uno specifico gruppo di trapiantati. Utilizzando la metodica IPlex Gold Mass Array Sequenom e tecniche di biologia molecolare convenzionale sono stati genotipizzati 26 antigeni minori di istocompatibilità per 46 coppie full-matched. Tutti i pazienti inclusi nel progetto di studio erano stati sottoposti a trapianto allogenico di cellule staminali emopoietiche da donatore familiare o volontario full-compatibile per leucemia mieloide cronica (n=46) o leucemia acuta linfoblastica Philadelphia positiva (LAL-Ph+, n=24). Il progetto ha confermato l'efficienza (98.6%) e la fattibilità delle metodiche proposte. Dal lavoro è inoltre emerso che, le differenze tra donatore e ricevente a libello mHAgs ACC-1, ACC-4, ACC-5, LB-MTHFD1-1Q, UGT2B17, DPH1, LRH1 potrebbero essere fattori predittivi di GvHD (p<0.05). La seconda evidenza è legata a un trend secondo cui il mismatch per LB-ADIR1 protegge dalla recidiva di malattia, in particolare nei confronti della LAL-Ph+ che è scarsamente responsiva all'allo-immunoterapia. Questo lavoro pilota, la cui casistica deve quindi essere ampliata, ha dimostrato l’efficacia della genotipizzazione con IPlex Gold Sequenom e l’elevato potenziale degli mHAgs sia come fattori predittivi di GvHD che come driver di GvL.
The outcome of allogeneic stem cell transplantation (Allo-SCT) is closely related to graft versus host disease (GvHD) and graft versus leukemia (GvL) effects which, in part, are mediated by mHAgs. Twenty-six mHAgs have been identified and reported to be differently and variably correlated with GVHD or GVL, but a simultaneous method to genotype a so large panel of mHAgs has never been employed. The aim of this work has been to develop a feasible method to genotype all the 26 mHAgs described so far and to test them for their correlation with GVHD and GVL in a group of donor/recipient pairs submitted to allo-SCT. For a multi-genotyping of 23 mHAgs we used iPlex Gold Mass Array technology (3 multiplex). For the other three mHAgs we designed other three assays based on conventional molecular biology. By these methods, we tested the 26 mHAgs in 46 donor/recipient pairs full-matched that underwent allo-SCT (sibling or MUD) because of Philadelphia positive CML (n=46) or ALL-Ph+ (n=24). Maldi-Tof IPlex Gold technology proved a high degree of efficiency (98.6%). As expected, sibling pairs showed most identity of MUD pairs. Notably, donor/recipient mismatch on ACC-1, ACC-4, ACC-5, LB-MTHFD1-1Q, UGT2B17, DPH1, LRH1 can drive GvHD effect (p<0.01). Next we identified that LB-ADIR1 can enhance (p=ns, but there is a trend) GvL effect specially on ALL-Ph+ that is otherwise un-responsible to allo-immunotherapy. Our data generated by a multi-genotype technique confirm the role of mHAgs in addressing GvL (in some cases without GvHD) and suggest that a study of mHAgs could be perfomed before transplant in order to better investigate the role of the known and new mHAgs involved in GvHD and GvL effects.
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Cattina, Federica <1983&gt. "Studio dei polimorfismi genici degli antigeni minori di istocompatibilità e GvHD/GvL nel trapianto allogenico di cellule staminali emopoietiche." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2013. http://amsdottorato.unibo.it/5672/.

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L'outcome dei pazienti sottoposti a trapianto allogenico di cellule staminali emopoietiche è fortemente influenzato da graft versus leukemia (GvL) e graft versus host disease (GvHD) che sono mediate, almeno in parte, dagli antigeni minori di istocompatibilità (mHAgs). In letteratura sono stati identificati 26 mHAgs che sono stati correlati a GvHD/GvL con risultati incompleti e in alcuni casi contrastanti; inoltre manca una metodica che sia in grado di genotipizzare contemporaneamente un pannello così ampio. Il lavoro è stato finalizzato alla preparazione di un protocollo di laboratorio che permetta di studiare in modo efficace i 26 mHAgs identificati, per poi correlarli con GvHD/GvL all’interno di uno specifico gruppo di trapiantati. Utilizzando la metodica IPlex Gold Mass Array Sequenom e tecniche di biologia molecolare convenzionale sono stati genotipizzati 26 antigeni minori di istocompatibilità per 46 coppie full-matched. Tutti i pazienti inclusi nel progetto di studio erano stati sottoposti a trapianto allogenico di cellule staminali emopoietiche da donatore familiare o volontario full-compatibile per leucemia mieloide cronica (n=46) o leucemia acuta linfoblastica Philadelphia positiva (LAL-Ph+, n=24). Il progetto ha confermato l'efficienza (98.6%) e la fattibilità delle metodiche proposte. Dal lavoro è inoltre emerso che, le differenze tra donatore e ricevente a libello mHAgs ACC-1, ACC-4, ACC-5, LB-MTHFD1-1Q, UGT2B17, DPH1, LRH1 potrebbero essere fattori predittivi di GvHD (p<0.05). La seconda evidenza è legata a un trend secondo cui il mismatch per LB-ADIR1 protegge dalla recidiva di malattia, in particolare nei confronti della LAL-Ph+ che è scarsamente responsiva all'allo-immunoterapia. Questo lavoro pilota, la cui casistica deve quindi essere ampliata, ha dimostrato l’efficacia della genotipizzazione con IPlex Gold Sequenom e l’elevato potenziale degli mHAgs sia come fattori predittivi di GvHD che come driver di GvL.
The outcome of allogeneic stem cell transplantation (Allo-SCT) is closely related to graft versus host disease (GvHD) and graft versus leukemia (GvL) effects which, in part, are mediated by mHAgs. Twenty-six mHAgs have been identified and reported to be differently and variably correlated with GVHD or GVL, but a simultaneous method to genotype a so large panel of mHAgs has never been employed. The aim of this work has been to develop a feasible method to genotype all the 26 mHAgs described so far and to test them for their correlation with GVHD and GVL in a group of donor/recipient pairs submitted to allo-SCT. For a multi-genotyping of 23 mHAgs we used iPlex Gold Mass Array technology (3 multiplex). For the other three mHAgs we designed other three assays based on conventional molecular biology. By these methods, we tested the 26 mHAgs in 46 donor/recipient pairs full-matched that underwent allo-SCT (sibling or MUD) because of Philadelphia positive CML (n=46) or ALL-Ph+ (n=24). Maldi-Tof IPlex Gold technology proved a high degree of efficiency (98.6%). As expected, sibling pairs showed most identity of MUD pairs. Notably, donor/recipient mismatch on ACC-1, ACC-4, ACC-5, LB-MTHFD1-1Q, UGT2B17, DPH1, LRH1 can drive GvHD effect (p<0.01). Next we identified that LB-ADIR1 can enhance (p=ns, but there is a trend) GvL effect specially on ALL-Ph+ that is otherwise un-responsible to allo-immunotherapy. Our data generated by a multi-genotype technique confirm the role of mHAgs in addressing GvL (in some cases without GvHD) and suggest that a study of mHAgs could be perfomed before transplant in order to better investigate the role of the known and new mHAgs involved in GvHD and GvL effects.
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LOCAFARO, GRAZIA. "In vitro generation and in vivo characterization of IL-10 engineered T cells suitable for adoptive immunotherapy." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2015. http://hdl.handle.net/10281/83945.

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Le Tr1 sono un subset di cellule regolatorie CD4+ indotte in periferia e caratterizzate dalla produzione di IL-10. Nell’ultimo decennio molte risorse sono state impiegate nella ricerca di metodi efficaci per la produzione di cellule Tr1 in vitro. Il nostro gruppo ha dimostrato che Tr1 antigene-specifiche possono essere ottenute in vitro mediante l’utilizzo di IL-10 o di cellule dendritiche tolerogeniche (DC-10). Trials clinici nell’ambito di trapianti allogenici di cellule staminali ematopoietiche (allo-HSCT) hanno dimostrato il basso rischio di terapie cellulari basate sull’uso di Tr1. Il limite dei metodi sopra citati è la presenza di una frazione di non Tr1 che potrebbe limitarne l'efficacia. Per cui abbiamo sviluppato un protocollo per generare Tr1 (CD4IL-10) utilizzando un vettore lentivirale (LV) che codifica per IL-10 e . Abbiamo dimostrato che forzando l’espressione di IL-10 in CD4+ umane si ottengono cellule con fenotipo e funzioni sovrapponibili a quelle delle Tr1, inclusa la capacità di eliminare cellule mieloidi. Inoltre, il trasferimento di cellule CD4IL-10 in topi immuno-deficienti sopprime la reazione di xeno-GvHD (Andolfi e Fousteri, Mol Ther 2012). Tuttavia, non è ancora chiaro se la terapia cellulare con CD4IL-10 può influenzare l’attività anti-leucemica (GvL). Gli obiettivi del progetto di dottorato sono: 1. Definire se la lisi delle CD4IL-10 è sovrapponibile a quello di Tr1 e convalidare l'uso di CD4IL-10 policlonali come terapia cellulare in modelli pre-clinici di GvL e GvHD; 2. Sviluppare un protocollo in vitro per generare cellule allo-specifiche Tr1-like lentivirale LV-IL-10. Per raggiungere il primo obiettivo, l'attività citotossica di cellule policlonali CD4IL-10 è stata testata contro un pannello di blasti primari. Studi in vitro dimostrano che l'attività litica di cellule CD4IL-10 è dipendente dall’attivazione mediata da molecole di HLA di classe I e dal rilascio di granzimaB; inoltre, è specifica nei confronti di cellule CD13+, e richiede l'adesione mediata dal CD54 e l’espressione di CD112 sui blasti. Inoltre, studi in vivo dimostrano che il trasferimento di cellule CD4IL-10 in modelli umanizzati impedisce la reazione di xeno-GvHD mediata da cellule T allogeniche, senza inibirne la loro attività antileucemica (GvL). Inoltre, le CD4IL-10 hanno un’attività anti-leucemica anche in vivo. Per raggiungere il secondo obiettivo, CD4+ sono state messe in coltura con mDC. Durante la seconda stimolazione, le cellule T sono state trasdotte con LV-IL-10. Le CD4IL-10 sono state isolate, espanse, e caratterizzate. Dopo stimolazione allo-specifica, le CD4IL-10 secernono livelli più elevati di IL-10 e comparabili di IFN-γ rispetto a cellule di controllo; inoltre, mostrano un fenotipo anergico e soppressivo. Nel complesso, i risultati di questi studi forniscono un razionale per l'uso di CD4IL-10 per inibire la reazione di GvHD, preservando la GvL a seguito di allo-HSCT per curare tumori mieloidi e rappresentano il primo passo per lo sviluppo di cellule Tr1 allo-specifiche e incrementerà l'utilizzo delle Tr1 come terapia per indurre tolleranza verso antigeni selezionati, riducendo la soppressione immunitaria generale.
T regulatory type 1 (Tr1) cells are a subset of CD4+ regulatory T (Treg) cells induced in the periphery and characterized by IL-10 production. During the last decade much effort has been dedicated to establish suitable methods for Tr1 cell generation in vitro for Treg-cell based therapy. We demonstrated that Tr1 cells can be generated in vitro in an antigen-specific manner with recombinant IL-10 or IL-10-producing tolerogenic DC-10. Proof-of-principle clinical trials in allo-HSCT demonstrated the safety of Treg-based cell therapy with these Tr1 cells. However, Tr1 cell cultures generated with the above mentioned methods include a fraction of non-Tr1 cells that may limit the efficacy of immunotherapy with Tr1 cells. To overcome this limitation we developed a protocol to generate Tr1 (CD4IL-10) cells using a Lentiviral Vector (LV) encoding for human IL-10 and , as marker gene. We showed that enforced IL-10 expression confers Tr1 phenotype and functions to human CD4+ T cells, including killing of myeloid cells. Moreover, adoptive transfer of CD4IL-10 cells into immune-deficient mice suppresses xeno-GvHD (Andolfi G. and Fousteri G., Mol Ther 2012). However, it is still unclear whether adoptive therapy with CD4IL-10 cells can affect Graft versus Leukemia (GvL) activity. The aims of my PhD project are: 1. to define whether killing mediated by CD4IL-10 cells is super-imposable to that of classical Tr1 cells and to validate the use of polyclonal CD4IL-10 cells as cell therapy in humanized pre-clinical models of GvL and GvHD; 2. to develop a new in vitro protocol to generate an homogeneous population of allo-antigen specific IL-10-producing Tr1 cells by LV-IL-10 gene transfer. To achieve the first aim the cytotoxic activity of polyclonal CD4IL-10 cells has been tested against a panel of primary blasts. In vitro studies show that the cytolysis of CD4IL-10 cells is HLA-class I- and granzyme B-dependent, is specific for CD13+ cells, and requires CD54-mediated adhesion and CD112 expression on target primary leukemic blasts. Moreover, in vivo studies show that adoptive transfer of CD4IL-10 cells in humanized models prevents xeno-GvHD mediated by human allogeneic T cells, while sparing their GvL capacity. In addition, we prove that CD4IL-10 T cells have potent anti-leukemia effects also in vivo. To achieve the second aim human naive CD4+ T cells were co-cultured with allogeneic in vitro differentiated mature DC. During second stimulation T cells are transduced with LV-IL-10, and CD4IL-10 cells are selected, expanded, and functionally characterized. Upon allo-antigen specific stimulation, CD4IL-10 cells secrete significantly higher levels of IL-10 and comparable amounts of IFN- compared to control cells, and display an anergic and suppressive phenotype. Overall, results from these studies provide a strong rationale for the use of CD4IL-10 cells to prevent GvHD while preserving GvL in allo-HSCT to cure myeloid malignancies and represent the first step for the development of allo-antigen specific Tr1 cells and will contribute to increase the use of Tr1-based immunotherapy, inducing tolerance to selected antigens, while minimizing general immune suppression.
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Heidenreich, Martin [Verfasser], and Matthias [Akademischer Betreuer] Edinger. "Auswirkungen einer GVHD auf das B-Zell-Kompartiment und die Bedeutung indirekter GVL-Effekte gegen B-Zell-Lymphome / Martin Heidenreich ; Betreuer: Matthias Edinger." Regensburg : Universitätsbibliothek Regensburg, 2021. http://d-nb.info/1231076143/34.

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Wermuth, Marieke [Verfasser], Gerald [Akademischer Betreuer] Wulf, and Tim [Akademischer Betreuer] Beissbarth. "Die Rolle von Zytokin- und Zytokinrezeptorgenvariationen für die Ausprägung von GvHD und GvL nach allogener Blutstammzelltransplantation bei Patienten mit hämatologischer Neoplasie / Marieke Wermuth. Gutachter: Gerald Wulf ; Tim Beissbarth. Betreuer: Gerald Wulf." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2014. http://d-nb.info/1048219739/34.

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Gonçalves, Alice Dahmer. "Caracterização das células natural killer (NK) circulantes no sangue periférico precocemente após o transplante de células-tronco hematopoéticas (TCTH)." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2017. http://hdl.handle.net/10183/179881.

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O transplante de células-tronco hematopoéticas alogênico (alo-TCTH) é uma opção de tratamento para uma variedade de doenças neoplásicas e não neoplásicas, principalmente de origem hematológica sendo doença do enxerto-contra-hospedeiro (DECH) a sua principal complicação. As células Natural Killer (NK) são os primeiros linfócitos a se recuperarem após o TCTH. Além da capacidade de promover o efeito enxerto-versus-leucemia (EVL), as células NK do doador parecem capazes de promover a pega do enxerto e de prevenir o desenvolvimento da DECH. As células NK compreendem aproximadamente 10% dos linfócitos do sangue periférico e são caracterizadas fenotipicamente pela expressão do antígeno de superfície CD56 (CD, cluster of differentiation) e pela ausência de CD3 (CD56+CD3-). O subtipo de células NK CD56dim (baixa densidade do antígeno) é naturalmente mais citotóxico que o subtipo CD56bright (alta densidade do antígeno) o qual é caracterizado pela capacidade de produção de citocinas. Com base nisso, o objetivo do trabalho é avaliar a presença de células NK nos dias 7, 14, 21 e 28 após o TCTH alogênico e autólogo, caracterizando sua frequência, seu imunofenótipo e a sua capacidade de produzir fatores de crescimento hematopoético e citocinas relacionadas.
Allogeneic hematopoietic stem cell transplantation (allo-HSCT) is an option of treatment for a variety of neoplastic and non-neoplastic diseases and graft-versus-host disease (GVHD) is its main complication. Natural Killer cells (NK) are the first lymphocytes to recover after HSCT. In addition to the ability to promote graft versus leukemia effect (GVL), donor NK cells appear to be capable of promoting engraftment and preventing the development of GVHD. NK cells comprise approximately 10% of peripheral blood lymphocytes and are characterized phenotypically by the expression of the CD56 surface antigen and absence of CD3 (CD56 + CD3-). The CD56dim (low density of antigen) NK cell subtype is naturally more cytotoxic than the CD56bright (high density of antigen) subtype which is characterized by the ability to produce cytokines. Based on this, the objective of the study is to evaluate the presence of NK cells on days 7, 14, 21 and 28 after allogeneic and autologous HSCT, characterizing their frequency, their immunophenotype and their capacity to produce hematopoietic growth factors and related cytokines.
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Forcade, Edouard. "Immunobiologie de la GVH chronique humain : dérégulation de la réaction du centre germinatif et implication de la réponse Th17." Thesis, Bordeaux, 2016. http://www.theses.fr/2016BORD0439/document.

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La GVH chronique (cGVHD) est une complication fréquente de l’allogreffe de cellules souches hématopoïétiques (CSH) dont la physiopathologie demeure partiellement comprise. Les données disponibles ont établi le rôle des lymphocytes T (LT) et B (LB) au cours de la cGVHD, mais la qualité de leur interaction et les sous-types de LT impliqués restent à définir. L’interaction entre les LT et les LB se fait au niveau du centre germinatif (CG) aboutissant à la production de LB mémoires et de cellules productrices d’anticorps de haute affinité grâce aux signaux d’aide reçus par les LT folliculaires helpers (TFH) finement contrôlés par une population régulatrice (TFR). La possibilité d’interroger les évènements se déroulant au niveau du CG par l’analyse de leur contingent circulant (c) nous a permis de mieux comprendre la physiopathologie de la cGVHD. En effet, la signature phénotype des cTFH suggère un gain de fonction au cours de la cGVHD, confirmée par étude fonctionnelle, et corrélant avec le phénotype des LB observé. De plus, les mécanismes de régulation apparaissent défectueux au cours de la cGVHD, puisque les cTFR présentent un défaut numérique expliqué par un défaut de résistance à l’apoptose et de prolifération. D’autre part, nous avons analysé une population de LT CD4+CD146+CCR5+, leur conférant une capacité de migration au travers des structures endothéliales et vers les sites inflammatoires. Cette population est significativement augmentée au cours de la cGVHD, et les modèles murins de cGVHD recevant des splénocytes de souris CD146-/- voient leur score clinique amélioré. L’expression de CD146 est associée à une polarisation Th17 justifiant un traitement par TMP778 (inhibiteur de RORγt) améliorant la cGVHD chez la souris. L’analyse de ces populations révèle des anomalies de la balance effecteurrégulateur et de potentielles cibles thérapeutiques à évaluer en clinique
Chronic GVHD (cGVHD) remains a major complication of allogeneic stem cell transplantation and its pathogenesis poorly understood. Previous reports established the role of T cells and B cells during cGVHD, but the quality of their interaction and T cell subsets involved remain to be defined. T cell – B cell crosstalk occurs in the germinal center generating memory B cells and high affinity antibody secreting cells consecutively to signals provided by T follicular helper cells (TFH) which are tightly controlled by a regulatory subset (TFR). The opportunity to interrogate events occurring in the germinal center through the analysis of their circulating contingent (c), allowed us to better understand cGVHD pathogenesis. cTFH phenotypic signature suggest an enhanced function during cGVHD, confirmed in functional studies, and correlating with observed B cell phenotype. In addition, regulatory mechanisms appeared defective during cGVHD, as cTFR showed a numerical deficiency, explained by a defect in resistance to apoptosis and low proliferative capacity. We also studied a T cell subset expressing CD4+CD146+CCR5+, giving the capacity to migrate through endothelial structures and toward inflammatory sites. This population is significantly increased during cGVHD, and cGVHD murine models receiving splenocytes from CD146-/- mice showed improved clinical score. CD146 expression is associated with a Th17 polarization justifying a treatment by TMP778 (RORγt inhibitor) improving cGVHD in mice. The analysis of these different populations revealed an abnormal effector-regulator balance and potential therapeutic targets to evaluate in clinic
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Books on the topic "GvL and GvHD"

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Toubai, Tomomi, and Robert Zeiser, eds. Cutting-Edge Translational Research in Graft-Versus-Host Disease (GVHD) and Graft-Versus-Tumor (GVT) Effect After Allogeneic Hematopoietic Cell Transplantation. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88976-488-4.

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Book chapters on the topic "GvL and GvHD"

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Martelli, Massimo F., Mauro Di Ianni, and Loredana Ruggeri. "Adoptive Immunotherapy with Regulatory and Conventional T-cells in Haploidentical T-cell Depleted Transplantation Protects from GvHD and Exerts GvL Effect." In Haploidentical Transplantation, 43–54. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-54310-9_4.

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Szatmári, S., T. Nagy, P. Simon, and M. Feuerhake. "GVD-Compensated Pump-Probe Apparatus." In Ultrafast Processes in Spectroscopy, 621–22. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4615-5897-2_138.

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Gooch, Jan W. "Graft-Versus-Host (GVH) Disease." In Encyclopedic Dictionary of Polymers, 896. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_13856.

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Schmitt, M., Y. Miyahara, X. Gu, K. Mukae, K. Satoh, E. Nakayama, L. Bergmann, and H. Shiku. "Differential Enhancement of Graft-Versus-Host (GVH) and Graft-Versus-Leukemia (GVL) Reactions by Interleukin-12 (IL-12)." In Molecular Biology of Hematopoiesis 6, 83–89. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4797-6_11.

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Markey, Kate A., Shuichiro Takashima, Alan M. Hanash, and Geoffrey R. Hill. "Cytokines in GVHD and GVL." In Immune Biology of Allogeneic Hematopoietic Stem Cell Transplantation, 293–322. Elsevier, 2019. http://dx.doi.org/10.1016/b978-0-12-812630-1.00017-7.

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"Separating GVHD and GVL Reactions." In Allogeneic Immunotherapy for Malignant Diseases, 297–318. CRC Press, 2000. http://dx.doi.org/10.1201/9780203909508-18.

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Barrett, John, and Dimitrios Mavroudis. "Separating GVHD and GVL Reactions." In Allogeneic Immunotherapy for Malignant Diseases. CRC Press, 2000. http://dx.doi.org/10.1201/9780203909508.pt3.

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Michonneau, David, Philippe Bousso, and Robert S. Negrin. "In Vivo Imaging of GVHD and GVL." In Immune Biology of Allogeneic Hematopoietic Stem Cell Transplantation, 51–68. Elsevier, 2019. http://dx.doi.org/10.1016/b978-0-12-812630-1.00004-9.

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Arvindam, Upasana Sunil, Ethan George Aguilar, Martin Felices, William Murphy, and Jeffrey Miller. "Natural Killer Cells in GvHD and GvL." In Immune Biology of Allogeneic Hematopoietic Stem Cell Transplantation, 275–92. Elsevier, 2019. http://dx.doi.org/10.1016/b978-0-12-812630-1.00016-5.

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"T-Cell Subsets and Separation of GVL from GVHD." In Allogeneic Immunotherapy for Malignant Diseases, 319–26. CRC Press, 2000. http://dx.doi.org/10.1201/9780203909508-19.

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Conference papers on the topic "GvL and GvHD"

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Danielius, Romas, Paolo Di Trapani, Audrius Dubietis, and Gintaras Valiulis. "Tilted pulses and X(2) cascading: effects on transient compression and temporal-soliton formation." In The European Conference on Lasers and Electro-Optics. Washington, D.C.: Optica Publishing Group, 1998. http://dx.doi.org/10.1364/cleo_europe.1998.cwh6.

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In X(2) cascading, two relevant phenomena are expected in case of suitable group-velocity mismatch (GVM) and group-velocity dispersion (GVD) material parameters: (i) if the GVM dominates and the low-frequency pulses run with opposite velocities respect to the high-frequency one, then interaction could lead to the so called “non-linear transient pulse compression” or to the elastic scattering of non-trapped soliton pulses, (ii) If the GVD dominates and has the same sign for all three waves, then mutually-trapped dispersion-free bright solitons (or quasi-solitons) are attained, due to the interplay between GVD and nonlinearity. Unfortunately, such operating conditions are hardly achievable in real experiments. Non-linear pulse compression was demonstrated only for very specific crystals and wavelengths; regarding the GVD solitons, they are commonly considered as not obtainable due to the low intrinsic dispersion of available X(2) materials, which makes the GVM split the interacting pulses before the trapping mechanism sets in. For a review of the argument, see ref. [1] and references therein.
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Avrorin, Alexander, V. A.Allakhverdyan, А. D.Avrorin, A. V.Avrorin, V. M.Aynutdinov, R. Bannasch, Z. Bardаčová, et al. "Positioning system for Baikal-GVD." In 37th International Cosmic Ray Conference. Trieste, Italy: Sissa Medialab, 2021. http://dx.doi.org/10.22323/1.395.1083.

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Fajt, Lukas, Zh A. M. Dzhilkibaev, M. D. Shelepov, A. D. Avrorin, A. V. Avrorin, V. M. Aynutdinov, R. Bannash, et al. "The Baikal-GVD detector calibrations." In 36th International Cosmic Ray Conference. Trieste, Italy: Sissa Medialab, 2019. http://dx.doi.org/10.22323/1.358.0878.

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Suvorova, Olga. "Baikal-GVD: first cluster Dubna." In The European Physical Society Conference on High Energy Physics. Trieste, Italy: Sissa Medialab, 2016. http://dx.doi.org/10.22323/1.234.0418.

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Yang, Aiying, Anshi Xu, and Deming Wu. "GVD compensation schemes with conideration for the combined effects of GVD, Kerr effect, and PMD." In Asia-Pacific Optical and Wireless Communications 2002, edited by Shuisheng Jian, Steven Shen, and Katsunari Okamoto. SPIE, 2002. http://dx.doi.org/10.1117/12.481198.

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Avrorin, A. D., A. V. Avrorin, V. M. Aynutdinov, R. Bannasch, I. A. Belolaptikov, D. Yu Bogorodsky, V. B. Brudanin, et al. "STATUS OF THE BAIKAL-GVD PROJECT." In 16th Lomonosov Conference on Elementary Particle Physics. WORLD SCIENTIFIC, 2015. http://dx.doi.org/10.1142/9789814663618_0019.

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Yang, Aiying, Deming Wu, and Anshi Xu. "GVD compensation schemes with considering PMD." In Proceedings of the First International Conference on ICOCN 2002. WORLD SCIENTIFIC, 2002. http://dx.doi.org/10.1142/9789812776280_0006.

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Aynutdinov, Vladimir, V. A. Allakhverdyan, A. D. Avrorin, A. V. Avrorin, R. Bannasch, Z. Bardаčová, I. A. Belolaptikov, et al. "Time synchronization of Baikal-GVD clusters." In 37th International Cosmic Ray Conference. Trieste, Italy: Sissa Medialab, 2021. http://dx.doi.org/10.22323/1.395.1067.

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Kim, Bok Young, Jae K. Jang, Yoshitomo Okawachi, Xingchen Ji, Michal Lipson, and Alexander L. Gaeta. "Synchronization of Normal-GVD Kerr Combs." In CLEO: Science and Innovations. Washington, D.C.: OSA, 2021. http://dx.doi.org/10.1364/cleo_si.2021.sw2h.3.

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Fajt, Lukas, A. D. Avrorin, A. V. Avrorin, Vladimir Aynutdinov, Rudolf Bannash, I. A. Belolaptikov, Victor Brudanin, et al. "Baikal-GVD: Time Calibrations in 2016." In 35th International Cosmic Ray Conference. Trieste, Italy: Sissa Medialab, 2017. http://dx.doi.org/10.22323/1.301.1036.

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Reports on the topic "GvL and GvHD"

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Mawassi, Munir, Adib Rowhani, Deborah A. Golino, Avichai Perl, and Edna Tanne. Rugose Wood Disease of Grapevine, Etiology and Virus Resistance in Transgenic Vines. United States Department of Agriculture, November 2003. http://dx.doi.org/10.32747/2003.7586477.bard.

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Abstract:
Rugose wood is a complex disease of grapevines, which occurs in all growing areas. The disease is spread in the field by vector transmission (mealybugs). At least five elongated-phloem- limited viruses are implicated in the various rugose wood disorders. The most fully characterized of these are Grapevine virus A (GV A) and GVB, members of a newly established genus, the vitivirus. GVC, a putative vitivirus, is much less well characterized than GV A or GVB. The information regarding the role of GVC in the etiology and epidemiology of rugose wood is fragmentary and no sequence data for GVC are available. The proposed research is aimed to study the etiology and epidemiology of rugose wood disease, and to construct genetically engineered virus-resistant grapevines. The objectives of our proposed research were to construct transgenic plants with coat protein gene sequences designed to induce post-transcriptional gene silencing (pTGS); to study the epidemiology and etiology of rugose wood disease by cloning and sequencing of GVC; and surveying of rugose wood- associated viruses in Californian and Israeli vineyards. In an attempt to experimentally define the role of the various genes of GV A, we utilized the infectious clone, inserted mutations in every ORF, and studied the effect on viral replication, gene expression, symptoms and viral movement. We explored the production of viral RNAs in a GV A-infected Nicotiana benthamiana herbaceous host, and characterized one nested set of three 5'-terminal sgRNAs of 5.1, 5.5 and 6.0 kb, and another, of three 3'-terminal sgRNAs of 2.2, 1.8 and 1.0 kb that could serve for expression of ORFs 2-3, respectively. Several GV A constructs have been assembled into pCAMBIA 230 I, a binary vector which is used for Angrobacterium mediated transformation: GV A CP gene; two copies of the GV A CP gene arranged in the same antisense orientation; two copies of the GV A CP gene in which the downstream copy is in an antigens orientation; GV A replicase gene; GV A replicase gene plus the 3' UTR sequence; and the full genome of GV A. Experiments for transformation of N. benthamiana and grapevine cell suspension with these constructs have been initiated. Transgenic N. benthamiana plants that contained the CP gene, the replicase gene and the entire genome of GV A were obtained. For grapevine transformation, we have developed efficient protocols for transformation and successfully grapevine plantlets that contained the CP gene and the replicase genes of GV A were obtained. These plants are still under examination for expression of the trans genes. The construction of transgenic plants with GV A sequences will provide, in the long run, a means to control one of the most prevalent viruses associated with grapevines. Our many attempts to produce a cDNA library from the genome of GVC failed. For surveying of rugose wood associated viruses in California vineyards, samples were collected from different grape growing areas and tested by RT-PCR for GV A, GVB and GVD. The results indicated that some of the samples were infected with multiple viruses, but overall, we found higher incidence of GVB and GV A infection in California vineyards and new introduction varieties, respectively. In this research we also conducted studies to increase our understanding of virus - induced rootstock decline and its importance in vineyard productivity. Our results provided supporting evidence that the rootstock response to virus infection depends on the rootstock genotype and the virus type. In general, rootstocks are differ widely in virus susceptibility. Our data indicated that a virus type or its combination with other viruses was responsible in virus-induced rootstock decline. As the results showed, the growth of the rootstocks were severely affected when the combination of more than one virus was present.
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