Готові списки джерел за темами / Allogeneic response

Добірка наукової літератури з теми "Allogeneic response"

Автор: Grafiati

Опубліковано: 10 грудня 2022

Оновлено: 28 січня 2023

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Статті в журналах з теми "Allogeneic response"

Hyc, Anna, Jacek Malejczyk, Anna Osiecka, and Stanislaw Moskalewski. "Immunological Response against Allogeneic Chondrocytes Transplanted into Joint Surface Defects in Rats." Cell Transplantation 6, no. 2 (March 1997): 119–24. http://dx.doi.org/10.1177/096368979700600205.

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Rat chondrocytes isolated from the articular–epiphyseal cartilage complex were transplanted into defects prepared in articular cartilage and subchondral bone. Transplants were taken for examination after 3 and 8 wk. Cartilage formed by syngeneic chondrocytes did not evoke formation of infiltrations. Contrary to that, in the vicinity of cartilage produced by allogeneic chondrocytes numerous infiltrating cells were present and cartilage resorption could be observed. Cyclosporine-A (CsA) treatment of recipients of allogeneic chondrocytes only partially suppressed accumulation of infiltrating cells and matrix resorption. Antichondrocyte immune response of chondrocyte graft recipients was studied by evaluation of spleen mononuclear cells (SMC) stimulation in mixed splenocytechondrocyte cultures and by evaluation of antichondrocyte cytotoxic antibodies. No difference in stimulation of SMC from intact rats by syngeneic and allogeneic chondrocytes was observed. Stimulation by allogeneic chondrocytes was slightly but significantly higher in recipients of syngeneic grafts. SMC of allogenic chondrocyte recipients were strongly stimulated by allogeneic chondrocytes. This response was absent in recipients treated with CsA. Spontaneous antichondrocyte cytotoxic antibody activity was detected in intact rats and in recipients of syngeneic grafts. In recipients of allogeneic chondrocytes the antibody response against allogeneic chondrocytes was raised but was statistically not significant owing to the considerable variation in the level of spontaneously occurring antichondrocyte antibodies.

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Martínez-Varea, Alicia, Begoña Pellicer, Alfredo Perales-Marín, and Antonio Pellicer. "Relationship between Maternal Immunological Response during Pregnancy and Onset of Preeclampsia." Journal of Immunology Research 2014 (2014): 1–15. http://dx.doi.org/10.1155/2014/210241.

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Maternofetal immune tolerance is essential to maintain pregnancy. The maternal immunological tolerance to the semiallogeneic fetus becomes greater in egg donation pregnancies with unrelated donors as the complete fetal genome is allogeneic to the mother. Instead of being rejected, the allogeneic fetus is tolerated by the pregnant woman in egg donation pregnancies. It has been reported that maternal morbidity during egg donation pregnancies is higher as compared with spontaneous orin vitrofertilization pregnancies. Particularly, egg donation pregnancies are associated with a higher incidence of pregnancy-induced hypertension and placental pathology. Preeclampsia, a pregnancy-specific disease characterized by the development of both hypertension and proteinuria, remains the leading cause of maternal and perinatal mortality and morbidity. The aim of this review is to characterize and relate the maternofetal immunological tolerance phenomenon during pregnancies with a semiallogenic fetus, which are the spontaneously conceived pregnancies andin vitrofertilization pregnancies, and those with an allogeneic fetus or egg donation pregnancies. Maternofetal immune tolerance in uncomplicated pregnancies and pathological pregnancies, such as those with preeclampsia, has also been assessed. Moreover, whether an inadequate maternal immunological response to the allogenic fetus could lead to a higher prevalence of preeclampsia in egg donation pregnancies has been addressed.

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Fabre, John W. "The allogeneic response and tumor immunity." Nature Medicine 7, no. 6 (June 2001): 649–52. http://dx.doi.org/10.1038/89008.

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Jones, RJ, RF Ambinder, S. Piantadosi, and GW Santos. "Evidence of a graft-versus-lymphoma effect associated with allogeneic bone marrow transplantation." Blood 77, no. 3 (February 1, 1991): 649–53. http://dx.doi.org/10.1182/blood.v77.3.649.649.

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Abstract The existence of an immunologic antileukemia reaction associated with allogeneic bone marrow transplantation (BMT) is well established. However, a similar graft-versus-tumor effect against lymphomas has not been demonstrated. We analyzed the results of BMT in 118 consecutive patients with relapsed Hodgkin's disease or aggressive non-Hodgkin's lymphoma. The 38 patients less than 50 years of age with HLA-matched donors had allogenic marrow transplants, and the other 80 patients received purged autologous grafts. The median age was 26 years in both the allogeneic and the autologous graft recipients. The patient's response to conventional salvage therapy before transplant was the only factor that influenced the event-free survival after BMT (P less than .001). Both the patient's response to salvage therapy before BMT (P less than .001) and the type of graft (P = .02) significantly influenced the probability of relapse after BMT. The actuarial probability of relapse in patients who responded to conventional salvage therapy before BMT was only 18% after allogenic BMT compared with 46% after autologous BMT. However, the actuarial probability of event-free survival at 4 years was the same, 47% versus 41%, for patients with responsive lymphomas who received allogeneic and autologous transplants, respectively (P = .8). The beneficial antitumor effect of allogeneic BMT was offset by its higher transplant-related mortality (P = .01), largely resulting from graft-versus-host disease. Allogeneic BMT appears to induce a clinically significant graft-versus- lymphoma effect. The magnitude of this effect is similar to that reported against leukemias.

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The existence of an immunologic antileukemia reaction associated with allogeneic bone marrow transplantation (BMT) is well established. However, a similar graft-versus-tumor effect against lymphomas has not been demonstrated. We analyzed the results of BMT in 118 consecutive patients with relapsed Hodgkin's disease or aggressive non-Hodgkin's lymphoma. The 38 patients less than 50 years of age with HLA-matched donors had allogenic marrow transplants, and the other 80 patients received purged autologous grafts. The median age was 26 years in both the allogeneic and the autologous graft recipients. The patient's response to conventional salvage therapy before transplant was the only factor that influenced the event-free survival after BMT (P less than .001). Both the patient's response to salvage therapy before BMT (P less than .001) and the type of graft (P = .02) significantly influenced the probability of relapse after BMT. The actuarial probability of relapse in patients who responded to conventional salvage therapy before BMT was only 18% after allogenic BMT compared with 46% after autologous BMT. However, the actuarial probability of event-free survival at 4 years was the same, 47% versus 41%, for patients with responsive lymphomas who received allogeneic and autologous transplants, respectively (P = .8). The beneficial antitumor effect of allogeneic BMT was offset by its higher transplant-related mortality (P = .01), largely resulting from graft-versus-host disease. Allogeneic BMT appears to induce a clinically significant graft-versus- lymphoma effect. The magnitude of this effect is similar to that reported against leukemias.

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Wu, Yongxia, Corey Mealer, Mohammed Sofi, Linlu Tian, David Bastian, Steven Schutt, Hee-Jin Choi, Chih-Hang Anthony Tang, Chih-Chi Andrew Hu, and Xue-Zhong Yu. "STING Negatively Regulates Allogeneic T Cell Responses by Constraining Function of Antigen Presenting Cells." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 87.11. http://dx.doi.org/10.4049/jimmunol.204.supp.87.11.

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Abstract Stimulator of interferon genes (STING) plays an important role in eliciting innate immune responses by sensing tumor and microbial DNA in anti-tumor and anti-infection responses, respectively. How the STING signal affects allogeneic response is not clear. To address this question, we utilized murine models of allogeneic hematopoietic stem cell transplantation (allo-HCT). By transferring donor bone marrow (BM) and T cells into allogeneic recipients, we found that significantly more severe graft-versus-host disease (GVHD) was induced in STING−/− recipients as compared to WT controls. By generating BM-chimeric mice in which STING was deficient in hematopoietic or non-hematopoietic antigen-presenting cells (APCs), we confirmed that STING on hematopoietic cells was primarily responsible for constraining host APC function. We further demonstrated that STING on host CD11c+ APCs played a predominant role in the regulation of allogenic T-cell responses. Mechanistically, we found that host CD11c+IAb+ cells deficient for STING could survive better and be activated more strongly after allo-HCT. As a consequence, STING-deficient APCs augmented donor T-cell expansion, chemokine receptor expression and migration into intestinal tissues, resulting accelerated/exacerbated GVHD after allo-HCT. Using pharmacologic approaches, we further demonstrated that systemic administration of STING agonist (c-diGMP) on recipient mice before irradiation significantly reduced GVHD mortality. In conclusion, we reveal a novel role of STING in APC activity that dictates T-cell allogenic responses, and validate STING as a potential therapeutic target for controlling GVHD after allo-HCT.

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Fedoseyeva, Eugenia V., Feng Zhang, Patricia L. Orr, David Levin, Harry J. Buncke, and Gilles Benichou. "De Novo Autoimmunity to Cardiac Myosin After Heart Transplantation and Its Contribution to the Rejection Process." Journal of Immunology 162, no. 11 (June 1, 1999): 6836–42. http://dx.doi.org/10.4049/jimmunol.162.11.6836.

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Abstract Allograft rejection is initiated by an immune response to donor MHC proteins. We recently reported that this response can result in breakdown of immune tolerance to a recipient self Ag. However, the contribution of this autoimmune response to graft rejection has yet to be determined. Here, we found that after mouse allogeneic heart transplantation, de novo CD4+ T cell and B cell autoimmune response to cardiac myosin (CM), a major contractile protein of cardiac muscle, is elicited in recipients. Importantly, CM is the autoantigen that causes autoimmune myocarditis, a heart autoimmune disease whose histopathological features resemble those observed in rejected cardiac transplants. Furthermore, T cell responses directed to CM peptide myhcα 334–352, a known myocarditogenic determinant, were detected in heart-transplanted mice. No responses to CM were observed in mice that had received an allogeneic skin graft or a syngeneic heart transplant, demonstrating that this response is tissue specific and that allogeneic response is necessary to break tolerance to CM. Next, we showed that sensitization of recipient mice with CM markedly accelerates the rejection of allogeneic heart. Therefore, posttransplant autoimmune response to CM is relevant to the rejection process. We conclude that transplantation-induced autoimmune response to CM represents a new mechanism that may play a significant role in cardiac transplant rejection.

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Lakkis, F. G., and R. I. Lechler. "Origin and Biology of the Allogeneic Response." Cold Spring Harbor Perspectives in Medicine 3, no. 8 (August 1, 2013): a014993. http://dx.doi.org/10.1101/cshperspect.a014993.

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Bumgardner, G. L., J. Li, M. B. Heininger, D. Xia, J. Parker-Thornberg, C. G. Orosz, and R. M. Ferguson. "In vivo immune response to allogeneic hepatocytes." Transplantation Proceedings 29, no. 4 (June 1997): 2059–60. http://dx.doi.org/10.1016/s0041-1345(97)00230-3.

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Riteau, Beatrice, Catherine Menier, Iman Khalil-Daher, Christine Sedlik, Jean Dausset, Nathalie Rouas-Freiss, and Edgardo D. Carosella. "HLA-G inhibits the allogeneic proliferative response." Journal of Reproductive Immunology 43, no. 2 (July 1999): 203–11. http://dx.doi.org/10.1016/s0165-0378(99)00034-0.

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Більше джерел

Дисертації з теми "Allogeneic response"

Collazo, Ruiz Michelle Marie. "The Role of Tumor Suppressors, SHIP and Rb, in Immune Suppressive Cells." Scholar Commons, 2012. http://scholarcommons.usf.edu/etd/4016.

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Regulatory T cells (Tregs) and myeloid-derived suppressor cells (MDSC) have been extensively studied in the past 30-40 years. Their potent suppressive capacity shown in several pathological and clinical settings, such as cancer and transplantation, has made it evident that better understanding their development and function is critical. Specifically, Tregs play a pivotal role in preventing autoimmunity, graft-versus-host disease (GvHD), and organ graft rejection. We previously demonstrated that germline or induced SH2 domain-containing inositol 5-phosphatase (SHIP) deficiency in the host abrogates GvHD. Here we show that SHIP-deficiency promotes an increase of FoxP3+ cells in both the CD4+CD25+ and the CD4+CD25- T cell compartments with increased expression of Treg-associated markers. Importantly, SHIP-deficiency does not compromise Treg function. Interestingly, like conventional Tregs, SHIP-/- CD4+CD25- T cells are unresponsive to allogeneic stimulators and suppress allogeneic responses by T cells in vitro, and can mediate reduced lethal GvHD in vivo. Thus, SHIP limits the immunoregulatory capacity of CD4+ T cell, particularly in allogeneic settings. SHIP-deficiency expands the number of immunoregulatory cells in both the T lymphoid and myeloid lineages. Here, we examined if these increases are interrelated. Specifically, we found that myeloid specific SHIP-deficiency leads to expansion of both MDSC and Treg numbers. Conversely, T lineage specific ablation of SHIP leads to expansion of Treg numbers, but not expansion of MDSC, indicating an intrinsic role for SHIP in limiting Treg numbers. Interestingly, MDSC lack SHIP expression suggesting that another SHIP-deficient myeloid cell promotes MDSC and Treg expansion. Also, increased levels of G-CSF, a myelopoietic growth factor, in SHIP-/- mice may extrinsically promote MDSC expansion since we found that G-CSF is required for the expansion of splenic MDSC in mice with induced SHIP-deficiency. MDSC consist of two distinct subsets, granulocytic-MDSC (G-MDSC), and monocytic-MDSC (M-MDSC) that differ in morphology, phenotype, suppressive capacity and differentiation potential. Importantly, M-MDSC can further differentiate into dendritic cells, macrophages and preferentially into G-MDSC, in the presence of tumor-derived factors (TDF). The retinoblastoma gene (Rb1), a tumor suppressor gene and central regulator of the cell cycle and differentiation, has been shown to influence monocytic and neutrophilic lineage commitment and to limit myeloproliferative disease. Here, we examined the role of Rb1 in the biology of MDSC subsets in tumor-bearing mice. Firstly, M-MDSC expressed high levels of Rb1 which remained relatively stable in culture with GM-CSF. Conversely, freshly isolated G-MDSC initially expressed undetectable levels of Rb1 that increased over time in culture, which correlated with increased histone acetylation at the Rb1 promoter. This increased Rb1 expression and histone acetylation was accelerated by histone deacetylase inhibitors (HDACi) treatment, suggesting Rb1 expression may be controlled by histone modification. Furthermore, when treated with HDACi, M-MDSC did not differentiate into G-MDSC in culture, even with TDF present. Finally, induced Rb1 deficiency in vivo promoted an expansion of splenic CD11b+Ly6G+Ly6Clo cells, similar to G-MDSC in tumor-bearing mice. Although further studies are required, these results strongly suggest that Rb1, like SHIP, plays a role in MDSC accumulation, particularly G-MDSC in cancer.

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Laylor, Ruthline Maria. "Characterisation of host versus graft responses following allogeneic stem cell transplantation." Thesis, Imperial College London, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.417391.

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Dam, Noémie Thi Nhu Quynh. "Allogeneic cardiac stem/progenitor cells and innate immune and humoral responses." Thesis, Sorbonne Paris Cité, 2018. http://www.theses.fr/2018USPCC251.

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Dans une société vieillissante, les maladies cardiovasculaires comme l’infarctus du myocarde représentent un challenge pour le système de santé. Les cellules souches, qui ont le potentiel de régénérer/réparer les organes tout au long de notre vie, constituent un traitement thérapeutique prometteur. Les stratégies qui ont utilisé des cellules autologues se sont heurtées à des limites que n’ont pas les cellules allogéniques mais leur immunogénicité peut constituer un obstacle à leur utilisation. Notre objectif a été d’étudier l’interaction des cellules souches/progéniteurs cardiaques humaines (hCPC) avec le système immunitaire inné et humoral dans un contexte allogénique pour identifer les risques et/ou bénéfices d’une telle thérapie. Les résultats montrent que les hCPC sont faiblement susceptibles à la cytotoxicité des cellules NK et qu’elles peuvent moduler leur cytotoxicité et leur sécrétion de cytokines vers un profile antiinflammatoire. Au contraire, les hCPC peuvent être éliminées par CDC ou ADCC en présence de DSA-HLA-I mais pas de DSA-HLA-II. Les hCPC sont aussi capables de recruter des monocytes circulants. Elles peuvent promouvoir l’activation des monocytes ainsi que des macrophages M1 et M2a vers un profile anti-inflammatoire et immuno-régulateur. Elles orientent la différentiation de monocytes en cellules dendritiques vers un profile de macrophages anti-inflammatoires avec une fonction de présentation d’antigène réduite. En conclusion, les hCPC pourraient contribuer à la régulation de l’inflammation postinfarctus et à la régénération/réparation cardiaque en modulant l’activité des cellules immunitaires dans un contexte allogénique. Cependant, leur susceptibilité aux DSA-HLA pourrait nécessiter une sélection des donneurs pour éviter une rapide élimination
In an aging society, cardiovascular diseases such as myocardial infarction represent a major challenge for the health system. Since stem cells have the potential to regenerate/repair the organs throughout our life, they offer an attractive and promising solution. Strategies using autologous cells have showed constraints that have lead to the development of allogeneic therapies, but the immunogenicity of allogeneic cells might constitute a major hurdle we need to address for their safe clinical translation. We sought to investigate the interaction of allogeneic human cardiac stem/progenitor cells (hCPC) with the innate and humoral immune systems to identify the risks and/or benefits of such therapy. Our studies revealed that hCPC are weakly susceptible to NK cell-mediated cytotoxicity. They have the capacity to modulate their cytotoxicity and to switch their secretion of cytokines towards an anti-inflammatory profile. In contrast, the presence of DSA-HLA-I but not DSA-HLA-II in recipient sera could induce the elimination of hCPC by CDC and ADCC. hCPC are able to recruit circulating monocytes and fine-tune their activation towards an anti-inflammatory regulatory profile. They promote the differentiation/activation of M1 and M2a macrophages into an anti-inflammatory/immuneregulatory profile. They could bend the differentiation of monocytes to dendritic cells towards anti-inflammatory macrophage-like cells with impaired antigen-presenting function. Overall, hCPC might contribute to the regulation of post-infarct inflammation and cardiac regeneration/repair by modulating the activities of innate immune cells in an allogeneic context. However, their sensitization to DSA-HLA requires a selection of the donors to avoid a rapid elimination

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Cardozo, Daniela Maira 1984. "Importância das disparidades genéticas nos genes HLA e KIR na resposta de pacientes submetidos ao transplante alogênico de células progenitoras hematopoiéticas para o tratamento de doenças onco-hematologicas = Importance of genetic differences in HLA and KIR genes in the response of patients undergoing allogeneic hematopoietic stem cell transplantation for treatment of onco-hematological diseases." [s.n.], 2013. http://repositorio.unicamp.br/jspui/handle/REPOSIP/308649.

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Orientadores: Cármino Antonio de Souza, Jeane Eliete Laguila Visentainer
Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
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Resumo: No organismo humano, as moléculas HLA (Human Leukocyte Antigens) são proteínas expressas na superfície da maioria das células nucleadas e são codificadas por genes localizados no braço curto do cromossomo 6 na região do Complexo Principal de Histocompatibilidade (CPH). Essas proteínas são caracterizadas pelo alto grau de polimorfismo, e também faz a ligação com receptores KIR (Immunoglobulin-like Receptors), expressos nas células Natural Killer. Os receptores KIR, que reconhecem moléculas do complexo HLA de classe I, estão entre os principais receptores inibidores dos linfócitos NK. Células infectadas por vírus e células tumorais perdem ou têm diminuída a expressão de moléculas HLA de classe I e, por isso, são eliminadas pela ausência de ligação entre moléculas HLA e receptores KIR inibitórios. Atualmente, muitos estudos têm destacado a importância dos genes KIR e HLA no Transplante de Células Progenitoras Hematopoiéticas (TCPH). O TCPH é o tratamento de escolha para muitas doenças hematológicas e dependem de vários fatores incluindo o estágio da doença, o regime de condicionamento, a fonte de células, o grau de identidade HLA entre doador e receptor e o desenvolvimento da doença do enxerto contra o hospedeiro (DECH). Estudos recentes indicam que a presença de células NK alorreativas no enxerto representa um fator favorável à recuperação de pacientes, uma vez que essas células têm a capacidade de eliminar células tumorais residuais pela ausência ou diminuição da expressão de moléculas HLA e sem a indução da DECH. Também outros fatores podem estar envolvidos na resposta pós-transplante, como a presença e ausência de determinados alelos HLA e genes KIR, os quais podem estar ligados à melhor ou pior resposta pós-transplante. O primeiro ensaio investigou a associação entre HLA e a ocorrência da DECH aguda e crônica em pacientes que receberam transplante de células progenitoras hematopoiéticas HLA-idêntico, aparentados. No total, foram 176 pacientes que receberam o primeiro transplante entre 1997 e 2009. DECH aguda foi positivamente associada ao HLA-A10 (P = 0.0007), HLA-A26 (P = 0.002), B55 (P = 0.001), DRB1*15 (P = 0.0211) e DQB1*05 (P = 0.038), enquanto que HLA-B16 (P = 0.0333) foi mais frequente em pacientes sem DECH aguda. DECH crônica foi positivamente associada com HLA-A9 (P = 0.01) e A23 (P = 0.0292) e negativamente associada com HLA-A2 (P = 0.0031) e B53 (P = 0.0116). HLA-B35 (P = 0.0373), B49 (P = 0.0155) e B55 (P = 0.0024) foi alta em pacientes com DECH aguda grau 3 ou mais, do que os outros pacientes. Nos pacientes com DECH crônica extensa, HLA-A9 (P = 0.0004), A24 (P = 0.0059) e A26 (P = 0.0411) foi maior do que nos outros pacientes, enquanto HLA-A2 foi baixo (P = 0.0097). O objetivo do segundo ensaio foi avaliar as possíveis interações dos genes KIR e HLA com o curso clínico do transplante HLA compatível, aparentado e não depletado de linfócitos T, particularmente na doença do enxerto contra o hospedeiro (DECH) aguda e crônica, recaída, sobrevida global e sobrevida livre de evento. A maioria dos doadores (78%) apresentaram o haplótipo B do KIR enquanto que 22% apresentaram o haplótipo A. Dos pacientes que receberam o haplótipo A do doador, 90% tiveram DECH, aguda ou crônica, comparados com os que receberam o haplótipo B (58%) (dados não estatisticamente significantes). Não houve diferença significativa para recaída entre pacientes que receberam os haplótipo A ou B (27% vs 23%). Não houve diferença no desenvolvimento da DECH e recaída para os pacientes homozigotos (C1C1 ou C2C2) e heterozigotos (C1C2) e nem para aqueles com HLA-Bw4 presente e ausente. Também, a sobrevida global não foi diferente para os grupos de pacientes analisados. No entanto, houve forte correlação entre o grupo de pacientes heterozigotos para HLA-C (C1C2) e a incidência de DECH aguda e recaída. A SLE foi maior nos pacientes heterozigotos que não desenvolveram DECHa (p<0,0001). Resultados mostraram que as variantes de HLA podem influenciar na ocorrência de DECH em transplante alogênico, com doadores relacionados, HLA-idênticos, tanto como fatores de proteção, quanto como fatores de susceptibilidade. Ainda, a interação KIR/HLA tem impacto significante no resultado dos transplantes relacionados, HLA compatível, sem depleção de linfócitos T, influenciando na incidência de recaída e na ocorrência da DECH. Resultados mostraram que para o grupo heterozigoto (C1C2) a maioria dos pacientes não desenvolveu DECH aguda e apresentou maior SLE, sugerindo um possível efeito protetor para esse grupo
Abstract: In the human organism, the HLA (human leukocyte antigens) are proteins expressed on the surface of most nucleated cells and are encoded by genes located on the short arm of chromosome 6 in the region of the Major Histocompatibility Complex (MHC). These proteins are characterized by a high degree of polymorphism, and also make the connection with KIR (Immunoglobulin-like Receptors), expressed in Natural Killer cells. KIR receptors that recognize HLA molecules of class I are among the major inhibitory receptors of NK-cells. Virus infected cells and tumor cells have lost or diminished expression of HLA class I molecules and therefore are eliminated by the absence of binding between HLA molecules and inhibitory KIR receptors. Currently, many studies have highlighted the importance of KIR and HLA genes in Hematopoietic Stem Cell Transplantation (HSCT). HPCT is the treatment of choice for many hematological malignancies and depends on various factors including stage of disease, the conditioning regimen, the source of cells, the degree of identity between donor and recipient HLA and development of chronic graft-versus-host (GVHD). Recent studies indicate that the presence of alloreactive NK cells in the graft is a factor aiding the recovery of patients, since these cells have the ability to eliminate residual tumor cells by the absence or diminution of expression of HLA molecules and without inducing GVHD. Also other factors may be involved in response post-transplant, as the presence or absence of certain HLA genes and KIR, which can be connected to a better or worse response after transplantation. The first trial investigated the association between HLA and the occurrence of acute and chronic GVHD in patients receiving hematopoietic stem cell transplant HLA-identical related. In total, 176 patients who received a first transplant between 1997 and 2009. GVHD was positively associated with HLA-A10 (P = 0.0007), HLA-A26 (P = 0.002), B55 (P = 0.001), DRB1 * 15 (P = 0.0211) and DQB1 * 05 (P = 0.038), while that HLA-B16 (P = 0.0333) was more frequent in patients without acute GVHD. Chronic GVHD was positively associated with HLA-A9 (P = 0.01) and A23 (P = 0.0292) and negatively associated with HLA-A2 (P = 0.0031) and B53 (P = 0.0116). HLA-B35 (P = 0.0373), B49 (P = 0.0155) and B55 (P = 0.0024) was high in patients with acute GVHD grade 3 or more, than the other patients. In patients with extensive chronic GvHD, HLA-A9 (P = 0.0004), A24 (P = 0.0059) and A26 (P = 0.0411) was greater than in the other patients, whereas HLA-A2 was low (P = 0.0097). The objective of the second test was to evaluate the possible interactions of KIR and HLA genes with the clinical course of the transplant HLA compatible related and not depleted of T lymphocytes, particularly in chronic graft versus host disease (GVHD) acute and chronic relapse, survival overall and event-free survival. Most donors (78%) presented the KIR B haplotype while 22% were haplotype A. Of the patients who received the donor haplotype A, 90% had GvHD, acute or chronic, compared with those who received the haplotype B (58%) (data not statistically significant). There was no significant difference in relapse between patients who received the haplotype A or B (27% vs 23%). There was no difference in the development of GVHD and relapse for patients homozygous (C1C1 or C2C2) and heterozygous (C1C2) and not for those with HLA-Bw4 present and absent. Also, the overall survival was not different for the groups of patients studied. However, there was strong correlation between the group of patients heterozygous for HLA-C (C1C2) and the incidence of acute GVHD and relapse. The SLE was higher in patients who did not develop GVHD heterozygotes (p <0.0001). Results showed that the HLA variants may influence the occurrence of GVHD in allogeneic transplantation with related donors, HLA-identical, both as protective factors, such as susceptibility factors. Furthermore, the interaction KIR / HLA has a significant impact on the outcome of transplantation related HLA-compatible, without depletion of T cells, influencing the incidence of relapse and the occurrence of GVHD. Results showed that for the heterozygous group (C1C2) most patients did not develop acute GVHD and showed higher SLE, suggesting a possible protective effect for this group
Doutorado
Clinica Medica
Doutora em Clínica Médica

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Bertoni, Lélia. "Évaluation du potentiel thérapeutique des cellules souches mésenchymateuses dans un modèle d'arthropathie expérimentale induite chez le cheval Characterization and use of Equine Bone Marrow Mesenchymal Stem Cells in Equine Cartilage Engineering. Study of their Hyaline Cartilage Forming Potential when Cultured under Hypoxia within a Biomaterial in the Presence of BMP-2 and TGF-ß1 Intra-Articular Injection of 2 Different Dosages of Autologous and Allogeneic Bone Marrow- and Umbilical Cord-Derived Mesenchymal Stem Cells Triggers a Variable Inflammatory Response of the Fetlock Joint on 12 Sound Experimental Horses An experimentally induced osteoarthritis model in horses performed on both metacarpophalangeal and metatarsophalangeal joints: Technical, clinical, imaging, biochemical, macroscopic and microscopic characterization Evaluation of allogeneic bone-marrow-derived and umbilical cord blood-derived mesenchymal stem cells to prevent the development of osteoarthritis in an equine model Chondrogenic Differentiation of Defined Equine Mesenchymal Stem Cells Derived from Umbilical Cord Blood for Use in Cartilage Repair Therapy." Thesis, Normandie, 2020. http://www.theses.fr/2020NORMC417.

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’arthropathie dégénérative est une maladie ayant des répercussions socio-économiques majeures chez l’homme et le cheval. Il n’existe pour l’heure aucun traitement curatif de cette maladie, le cartilage articulaire étant dépourvu de pouvoir de cicatrisation spontané. De nombreux espoirs reposent sur l’utilisation de cellules souches mésenchymateuses (CSM), pour leur potentiel pro-régénératif et anti-inflammatoire. Le premier objectif de cette étude était d’évaluer la tolérance des CSM de sang de cordon ombilical (SCO) et de moelle osseuse (MO) dans des articulations saines. L’étude contrôlée en aveugle menée sur 12 chevaux expérimentaux a démontré que l’injection de CSM-MO provoquait significativement plus de signes de réaction inflammatoire que l’injection de CSM-SCO, et que l’injection des CSM, quelle que soit leur origine, provoquait une réaction inflammatoire discrète à modérée, supérieure à celle d’une injection de placébo, avec une grande variabilité individuelle de sensibilité à une même lignée de cellules. Le second objectif était d’évaluer l’efficacité des CSM-MO et -SCO dans un modèle d’arthropathie induite. L’étude contrôlée en aveugle menée sur 8 chevaux expérimentaux a mis en évidence une réduction significative de la progression des signes indicateurs d’arthropathie à l’imagerie après injection de CSM-MO allogéniques par rapport à l’injection du placébo. Ces résultats encourageants, à considérer à la lumière des limites des études menées, indiquent un effet bénéfique des CSM-MO allogéniques dans la prise en charge de l’arthrose chez le cheval. Ils soulignent la nécessité de poursuivre les recherches afin de confirmer ces résultats, et d’optimiser les effets des CSM à travers leur combinaison à un vecteur ou par une approche acellulaire avec administration des nanovésicules qu’elles sécrètent, et considérées être à l’origine de leurs effets thérapeutiques
Osteoarthritis is a common cause of pain and economic loss in both humans and horses. There is currently no curative treatment for osteoarthritis, because of the lack of spontaneous regenerative capacity of the articular cartilage. Mesenchymal stem cells (MSC) based regenerative medicine comes across as a promising strategy given their pro-regenerative and anti-inflammatory potential. The first objective of this study was to evaluate the safety of umbilical cord blood (UCB) and bone marrow (BM) derived MSC in healthy joints. The blind controlled study conducted on 12 experimental horses showed that the injection of BM-MSC caused significantly more signs of inflammatory reaction than the injection of UCB-MSC, and that the injection of MSC, regardless of their origin, caused a discrete to moderate inflammatory reaction, greater than that of the placebo, with great individual variability in sensitivity to the same cell line. The second objective was to evaluate the efficacy of BM-MSC and UCB-MSC in a model of induced osteoarthritis. The blind controlled study conducted on 8 experimental horses showed a significant reduction in the progression of osteoarthritis associated signs with imaging techniques after injection of allogeneic BM-MSC compared to placebo. These promising results, to be considered in light of the limitations of the studies, indicate a beneficial effect of allogeneic BM-MSC in the management of osteoarthritis in horses. They underline the need for further research to confirm these results, and to optimize the effects of MSC through their combination with a vector or through an acellular approach with administration of the nanovesicles they secrete that ared considered to be responsible for their therapeutic effects

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KÃ¶ksoy, Sadi. "Evaluation of some of the functional aspects of CD8+/cytotoxic T cell responses in viral and allogeneic models /." The Ohio State University, 2002. http://rave.ohiolink.edu/etdc/view?acc_num=osu1486457871785254.

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Berrie, Jennifer. "DISTINCT T CELL CLONES ARE ASSOCIATED WITH GRAFT-VERSUS-HOST DISEASE (GVHD), AND POTENTIALLY GRAFT-VERSUS-TUMOR (GVT), RESPONSES FOLLOWING ALLOGENEIC STEM CELL TRANSPLANTATION." VCU Scholars Compass, 2011. http://scholarscompass.vcu.edu/etd/2450.

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In patients undergoing hematopoietic stem cell transplantation (HSCT) with HLA-identical donors, genetic polymorphisms result in a mismatch between donors and recipients in their minor histocompatibility antigens (mHAgs), and tumors may also express tumor-associated antigens (TAA) that may not be abundantly present in the donors. Donor T cells can recognize such mHAgs and TAAs as foreign antigens and generate an objective response against hematologic malignancies in a graft-versus-tumor (GVT) effect. However, a major side effect of HSCT occurs when donor T cells are alloreactive against the recipients’ normal cells, leading to graft-versus-host disease (GVHD). The ability to identify T cell clones that are exclusively involved in the GVT or GVHD responses remains elusive. In this study, we looked at clonally-driven CD3+ T cells in patients with hematologic malignancies prior to and after transplantation. We identified Vbeta families of increased expression involved in GVHD or GVT responses, with Vbetas 4, 11, and 23 being associated with GVHD, Vbetas 9, 16, and 20 being associated with GVT, and Vbetas 2, 3, 7, 8, 12, 15, and 17 being involved in GVHD and/or GVT. We were also able to identify some of the Vbeta families that were increased in the peripheral blood at the site of GVHD. Furthermore, one of our twelve patients had donor lymphocyte infusions (DLIs) for treatment of relapse, from which we were able to observe oligoclonal T cells that emerged at the time of post-DLI remission and re-establishment of GVHD.

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Chen, Juchuan. "The response of rat foetuses to allogeneic lymphocytes." Phd thesis, 1990. http://hdl.handle.net/1885/142691.

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Murase, Tosei. "Roles of Notch and NF-kB signaling in allogeneic responses." Phd thesis, 2006. http://hdl.handle.net/1885/7166.

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The induction of robust allograft tolerance is the ultimate goal for clinical transplantation. Although studies have identified that dendritic cells (DCs) are important for induction of antigen-specific tolerance, the requirements for generating tolerogenic DCs are yet to be elucidated. Recently, it has been demonstrated the modulation of two signaling pathways, Notch and nuclear factor KB (NF-KB) can render DCs tolerogenic. The studies documented here examine (1) whether immature DCs over-expressing Notch-related molecules (Jagged-I, Delta-like-I (Dll-I), Lunatic Fringe (Ung) , and Manic Fringe (Mfng)) act as immunoregulatory DCs and promote allograft survival; and (2) whether DCs deficient in NF-KB signaling inhibit the alloreactive T cell response and promote allograft survival ... Although the potential for Notch signaling to promote alloantigen-specific tolerance remains unresolved, these studies suggest that inhibition of NF-KB signaling in DCs represent a potential approach for promoting allograft survival.

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Sukumaran, M. K. "Effect Of Heat Exposure On Allogeneic Cytotoxic T Lymphocyte Responses In Mice." Thesis, 1996. http://etd.iisc.ernet.in/handle/2005/1877.

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Книги з теми "Allogeneic response"

Tyndall, Alan, and Jacob M. van Laar. Stem cell therapies. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0085.

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Since the start of the international project in 1997, over 1500 patients have received a haematopoietic stem cell transplant (HSCT), mostly autologous, as treatment for a severe autoimmune disease, with overall 85% 5-year survival and 43% progression-free survival. Around 30% of patients in all disease subgroups had a complete response, often durable despite full immune reconstitution. In many cases, e.g. systemic sclerosis, morphological improvement such as reduction of skin collagen and normalization of microvasculature was documented, beyond any predicted known effects of intense immunosuppression alone. It is hoped that the results of the three running large prospective randomized controlled trials will allow modification of the protocols to reduce the high transplant-related mortality which relates to regimen intensity, age of patient, and comorbidity. Multipotent mesenchymal stromal cells (MSC) have been recently tested in various autoimmune diseases, exploiting their immune modulating properties and apparent low acute toxicity. MSC display immune privilege in that the patient requires no immunosuppression prior to allogeneic MSC infusion. Despite encouraging small phase I/II studies, no positive data from randomized prospective studies are as yet available in the peer-reviewed literature.

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Tyndall, Alan, and Jacob M. van Laar. Stem cell therapies. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0085_update_003.

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Since the start of the international project in 1997, over 2000 patients have received a haematopoietic stem cell transplant (HSCT), mostly autologous, as treatment for a severe autoimmune disease, with overall 85% 5-year survival and 43% progression-free survival. Around 30% of patients in all disease subgroups had a complete response, often durable despite full immune reconstitution. In many cases, e.g. systemic sclerosis, morphological improvement such as reduction of skin collagen and normalization of microvasculature was documented, beyond any predicted known effects of intense immunosuppression alone. It is hoped that the results of the three running large prospective randomized controlled trials will allow modification of the protocols to reduce the high transplant-related mortality which relates to regimen intensity, age of patient, and comorbidity. Multipotent mesenchymal stromal cells (MSC) have been recently tested in various autoimmune diseases, exploiting their immune modulating properties and apparent low acute toxicity. MSC display immune privilege in that the patient requires no immunosuppression prior to allogeneic MSC infusion. Despite encouraging many small phase I/II studies, only 2 prospective controlled trials which achieved their primary endpoints have been published.

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Levy, Sharon. The effect of 3,3',4,4',5,5'-hexachlorobiphenyl on production of interleukins 1 and 2 and lymphocyte proliferation in an allogenic response. 1988.

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Levy, Sharon. The effect of 3,3',4,4',5,5'-hexachlorobiphenyl on production of interleukins 1 and 2 and lymphocyte proliferation in an allogenic response. 1988.

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Sterling, Katherine. The role of CD8+ T cells in the regulation of recipient immune responses induced by allogeneic platelet transfusions. 2004.

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Young, Kevin J. The role and mechanisms of CD3+CD4-CD8-regulatory T cells in the suppression of allogeneic immune responses. 2003.

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Частини книг з теми "Allogeneic response"

Bellucci, Roberto, and Edwin P. Alyea. "Harnessing Allogeneic Immunity for Anti-myeloma Response." In Advances in Biology and Therapy of Multiple Myeloma, 111–29. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-5260-7_5.

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Langrehr, J. M., J. Stadler, T. R. Billiar, H. Schraut, R. L. Simmons, and R. A. Hoffman. "Nitric Oxide Synthesis in Sponge Matrix Allografts Coincides with the Initiation of the Allogeneic Response." In Host Defense Dysfunction in Trauma, Shock and Sepsis, 471–75. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-77405-8_57.

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Buelens, Christel, Fabienne Willems, Géraldine Pierard, Anne Delvaux, Thierry Velu, and Michel Goldman. "IL-10 Inhibits the Primary Allogeneic T Cell Response to Human Peripheral Blood Dendritic Cells." In Advances in Experimental Medicine and Biology, 363–65. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1971-3_81.

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Taflin, Cécile, Benoit Favier, Dominique Charron, Denis Glotz, and Nuala Mooney. "Study of the Allogeneic Response Induced by Endothelial Cells Expressing HLA Class II After Lentiviral Transduction." In Antigen Processing, 461–72. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-218-6_34.

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Manier, Salomon, Artur Jurczyszyn, and David H. Vesole. "Bridging Chemotherapy: Multiple Myeloma." In The EBMT/EHA CAR-T Cell Handbook, 127–29. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-94353-0_24.

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AbstractIn the phase 2 KarMMa study, 88% of the patients received bridging therapy with only a 5% response (Munshi et al. 2021). In the CARTITUDE 1 trial, 75% of the patients received bridging therapy, with a reduction in tumour burden observed in 34% of the patients prior to cilta-cel infusion, but no patients achieved a CR or better while on bridging therapy (Madduri et al. 2019). Bridging therapy is recommended for virtually all patients. An exception can be discussed for patients with slowly progressive disease, who may not need to receive bridging therapy after leukapheresis; however, this strategy exposes them to a risk of rapid progression later during the manufacturing period. In the future, with allogeneic CAR-T cells, bridging therapy will likely not be necessary because the time between patient inclusion and CAR-T cell infusion is much reduced.

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Arnold, R., D. Bunjes, B. Hertenstein, C. Duncker, J. Novotny, M. Stefanic, M. Theobald, G. Heil, M. Wiesneth, and H. Heimpel. "Allogeneic BMT in Patients with AML: Influence of the Prior Response to Induction Chemotherapy on Outcome After BMT." In Acute Leukemias V, 380–82. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-78907-6_63.

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Ayodele, Olubukola, and Lillian L. Siu. "New Drugs for Recurrent or Metastatic Nasopharyngeal Cancer." In Critical Issues in Head and Neck Oncology, 337–52. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-63234-2_23.

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AbstractChemotherapy has been the backbone for the treatment of recurrent or metastatic nasopharyngeal carcinoma (RMNPC), which remains an incurable disease. Currently the most active area of therapeutic investigations in RMNPC is in immunotherapy, especially after the results of five anti-programmed death-1 (anti-PD-1) antibodies, i.e. pembrolizumab, nivolumab, camrelizumab, toripalimab and tislelizumab, have demonstrated monotherapy objective response rates of 21%–43%. Combinations using anti-PD1/L1 antibodies as backbone to evaluate their additivity or synergy with cytotoxic chemotherapy, molecularly targeted agents, or other immuno-oncology compounds are actively being developed. Besides immune checkpoint blockade, additional ways to modulate the host immune system, such as Epstein-Barr virus (EBV)-directed vaccination against viral antigens (such as EBNA1, LMP1, LMP2) with dendritic cells or peptides, adoptive cell transfer of autologous or HLA-matched allogeneic EBV-specific cytotoxic T lymphocytes, CAR or TCR T-cell therapy, personalized cancer vaccines and oncolytic viruses are being explored. Finally, novel molecularly targeted agents that have entered human testing in RMNPC include apatinib and anlotinib (antiangiogenic agents), MAK683 (an embryonic ectoderm development or EED protein inhibitor), among others. This review provides an update of ongoing clinical trials evaluating these new compounds in RMNPC.

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Blaise, Didier, and Sabine Fürst. "Post-CAR-T Cell Therapy (Consolidation and Relapse): Lymphoma." In The EBMT/EHA CAR-T Cell Handbook, 169–71. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-94353-0_33.

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AbstractEven after a decade of use, CAR-T cell therapy for non-Hodgkin lymphoma (NHL) is still evolving, and disease control is now the main concern in the majority of experienced centres. Indeed, despite highly appealing objective response (OR) rates in refractory patients, the long-term overall survival (OS) of this population has only slightly improved. Pivotal studies have suggested that 2-year OS rates do not surpass 30%, even though results improve when complete response (CR) is achieved within the first 3 months after treatment (Wang et al. 2020; Schuster et al. 2019; Neelapu et al. 2017). Although achieving this exceptionally high level of OR is praiseworthy, similar improvements have not been made regarding OS, and current OS probabilities are not satisfactory. Of course, there are multiple reasons for this; a substantial proportion of patients either do not achieve an initial response or experience progression very soon after treatment, with poor OS (Chow et al. 2019). Both populations present with disease burden or aggressive cancer prior to CAR-T cell therapy, possibly having been referred too late in the course of treatment or waited too long before CAR-T cells were processed for them. Both of these issues have potential solutions, such as more widely publicizing the efficacy of CAR-T cells, which may increase referrals at an earlier stage, and developing methods, which are already being heavily investigated, for shortening the manufacturing process (Rafiq et al. 2020). In the latter case, the use of allogeneic lymphocytes could allow for already prepared cells to be readily used when needed and would most likely be the most efficient strategy as long as the risk of graft-versus host disease is offset (Graham and Jozwik 2018). Thus, achieving CR is a crucial step in increasing OS, as patients with partial response (PR) or stable disease (SD) present with lower OS, while currently, recurrence appears to be rare when CR is maintained for more than 6 months (Komanduri 2021). However, the disease will likely recur in more than half of patients in the months following treatment, possibly due to issues such as the poor persistence of CAR-T cells (which may not be as crucial as once thought for acute lymphoblastic leukaemia (Komanduri 2021)) or the loss of target antigen expression (which has been regularly documented (Rafiq et al. 2020)). Both of these mechanisms could potentially be used to develop methods that reduce recurrence after CAR-T cell therapy. In fact, the most popular approaches currently being investigated are attempting to either use two CAR-T cell types that each target different antigens or to create CAR-T cell constructs that target either multiple antigens or an antigen other than CD19 (Shah et al. 2020). The concomitant infusion of CAR-T cells with targeted therapies is also being explored in other B-cell malignancies and appears to both increase the CR rate and decrease recurrence (Gauthier et al. 2020). When recurrence does occur, patient OS is rather dismal, and the best remaining option would most likely be inclusion in a clinical trial. If this option is not available, salvage therapy may be attempted, although cytotoxic treatments are extremely limited given that most diseases have been refractory to numerous lines of treatment prior to immunotherapy. A few case reports and studies with a small patient population receiving anti-PD-1 antibodies, ibrutinib, or ImiDs have been reported with largely anecdotal supporting evidence (Byrne et al. 2019). However, even in the case of a new objective response (OR), the subsequent risk of recurrence is substantial and may invite further consolidation with allogeneic haematopoietic stem cell transplantation (Byrne et al. 2019), which has already been performed in patients treated for acute lymphoblastic leukaemia (Hay et al. 2019). However, the efficacy of this strategy remains to be validated in NHL patients in clinical trials. Further supporting evidence, although limited, has recently been reported concerning an additional treatment with CAR-T cells inducing an OR. Of the 21 NHL patients included in the study, the OR rate after the second infusion was 52% (CR, n = 4; PR, n = 7), with some durable responses inviting further investigations (Gauthier et al. 2021). Overall, with such poor outcomes after recurrence, current efforts are also focused on predicting the patients most likely to experience disease progression and that are potential candidates for preemptive consolidation therapy, although there is no doubt that patients who do not achieve a rapid CR should be the first candidates. Additionally, immune monitoring should encompass not only CAR-T cell survival but also the detection of circulating tumour DNA (Komanduri 2021) because this could aid in detecting subclinical recurrence and in deciding whether consolidation or maintenance therapy should be administered. However, currently, all these approaches are highly speculative and require further clinical study.

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KIM, WONSUCK, ANDREW PETTER, KYLE STRAUB, and DAVID MOHRIG. "Investigating the autogenic process response to allogenic forcing." In From Depositional Systems to Sedimentary Successions on the Norwegian Continental Margin, 127–38. Chichester, UK: John Wiley & Sons, Ltd, 2014. http://dx.doi.org/10.1002/9781118920435.ch5.

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Müller, Gabriele, Joachim Saloga, Tieno Germann, Iris Bellinghausen, Mansour Mohamadzadeh, Jürgen Knop, and Alexander H. Enk. "Human Keratinocyte-Derived IL-12 Affects LC-Induced Allogeneic T-Cell Responses." In Advances in Experimental Medicine and Biology, 519–21. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1971-3_116.

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Тези доповідей конференцій з теми "Allogeneic response"

Aris, Mariana, María Betina Pampena, Estrella M. Levy, Alicia I. Bravo, Florencia P. Madorsky-Rowdo, Ana Mordoh, Julio Kaplan, et al. "Abstract A37: Immunization of cutaneous melanoma patients with the allogeneic cell vaccine CSF-470 enhances immune infiltration of metastatic lesions and would favor subsequent response to Vemurafenib." In Abstracts: AACR Special Conference: Tumor Immunology and Immunotherapy: A New Chapter; December 1-4, 2014; Orlando, FL. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/2326-6074.tumimm14-a37.

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Silva, Suresh de, George Fromm, Anandaroop Mukhopadhyay, Jean Campbell, Robert Pierce, and Taylor Schreiber. "Abstract 5617: Combined intratumoral electroporation and allogeneic vaccination of Gp96-Ig/Fc-OX40L stimulates CD8 T cell cross-priming to tumor specific neoantigens and enhanced anti-tumor response." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-5617.

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Gonzalez, Alba, Frances D. Liu, Archana Nagaraja, Alyssa Mullenix, Russell M. Gordley, Daniel O. Frimannsson, Anissa Benabbas, et al. "Abstract 4246: SENTI-101, a novel genetically modified allogeneic cell product expressing IL12 and IL21, elicits a tumor-localized, robust, and multimodal immune response in preclinical models of solid tumors." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-4246.

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Illarramendi, Jorge, María Carmen Mateos, Iván Quispe, María Cruz Viguria, María Teresa Zudaire, Amaya Zabalza, and Jose Juan Illarramendi. "MULTILINEAGE ACUTE LEUKEMIA DURING THE TREATMENT OF A PATIENT WITH BREAST CANCER WITH DOCETAXEL AND DOUBLE ANTI-HER2/NEU BLOCKADE: PERSPECTIVES AND POINTS TO CONSIDER." In Abstracts from the Brazilian Breast Cancer Symposium - BBCS 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s2065.

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Анотація:

Introduction: Associated or secondary acute leukemias (ALs) are rare complications after treatment of breast cancer (BC). There is no apparent increased risk of this complication with monoclonal anti-HER2/neu antibodies (AHAB), although most of them also receive topoisomerase inhibitors (TIs). We described the case of a patient who was diagnosed with AL during the combined treatment with two AHAB (trastuzumab [TTZ] and pertuzumab [PTZ]) without any TI. Case Report: A 64-year-old lady was diagnosed with stage IV HER2/neu-positive BC in April 2018. She received treatment with docetaxel plus PTZ and TTZ. Docetaxel was suspended after eight cycles with a complete radiological response (CR), and she continued receiving PTZ plus TTZ infusions every 3 weeks. In September 2020, an abnormal blood smear revealed a mixed AL, with features of myeloid, T-lymphoid, and B-lymphoid AL. The next-generation sequencing disclosed mutations in FLT3 and ASLX1. Imaging tests showed maintained CR of BC. She received induction and consolidation chemotherapy with fludarabine, cytarabine, and idarubicin, with confirmed CR by bone marrow examination and cytometry. After considering the high risk of AL relapse and good perspectives of maintaining CR of BC, a multidisciplinary conference agreed to offer allogeneic bone marrow transplantation (BMT) to the patient. She is now in the conditioning phase of the BMT. Conclusions: We have not found previous reports of mixed multilineage AL in patients with BC after treatment with AHAB so that no relation between them must be assumed at this time. The improved prognosis of metastatic BC with the addition of PTZ is a factor to take into account for the indication of treatments like BMT in cases of AL complicating this disease. A potential effect of graft versus BC has been described in some cases. The potential tolerance of AHAB after BMT is also another point for debate with limited evidence about it so far.

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Li, Y., J. Kim, T. Nguyen, C. Zhang, B. Cha, A. Birukova, and K. G. Birukov. "Contrasting Effects of Stored Allogeneic Red Blood Cells and Their Supernatants on Permeability and Inflammatory Responses in Human Pulmonary Endothelial Cells." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a5582.

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Lau, Sai Ping S., Priscilla P. Kinderman, Melanie M. Lukkes, Floris F. Dammeijer, Heleen H. Vroman, Menno M. van Nimwegen, Thorbald T. van Hall, et al. "Abstract B117: Allogeneic tumor-lysate loaded dendritic cells induce anti-tumor immunity and tumor responses in pre-clinical models of pancreatic adenocarcinoma: Towards clinical trials." In Abstracts: Fourth CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 30 - October 3, 2018; New York, NY. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr18-b117.

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Shawler, Daniel L., Alex Tong, Lily Liu, Ewa Carrier, Charles S. Davis, John Nemunaitis, and Habib Fakhrai. "Abstract 5364: Correlation of immune responses and overall survival in a phase II study of belagenpumatucel-L, an allogeneic tumor cell vaccine, in non-small cell lung cancer (NSCLC)." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-5364.

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Luo, Mengyao, Shamael S. Dastagir, Xuqing Zhang, Andrea Schmidt, Beatriz Marques, Timothy J. Lyford, Billy Blanco, Laurence A. Turka, Thomas J. Wickham, and Tiffany F. Chen. "Abstract PO044: RTX-321, an allogeneic red blood cell-based artificial antigen presenting cell, expressing MHC I-peptide, 4-1BBL and IL-12, engages primary human HPV-specific T cells and boosts other general immune responses." In Abstracts: AACR Virtual Special Conference: Tumor Immunology and Immunotherapy; October 19-20, 2020. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/2326-6074.tumimm20-po044.

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