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  • 1
    Online Resource
    Online Resource
    31st Annual Meeting and Associated Programs of the Society for Immunotherapy of Cancer (SITC 2016): part two : National Harbor, MD, USA. 9-13 November 2016
    BMJ ; 2016
    In:  Journal for ImmunoTherapy of Cancer Vol. 4, No. S1 ( 2016-11)
    Details
    In: Journal for ImmunoTherapy of Cancer, BMJ, Vol. 4, No. S1 ( 2016-11)
    Type of Medium: Online Resource
    ISSN: 2051-1426
    URL: Article
    DOI: 10.1186/s40425-016-0173-6
    Language: English
    Publisher: BMJ
    Publication Date: 2016
    detail.hit.zdb_id: 2719863-7
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  • 2
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    Online Resource
    The effect of mouse cytomegalovirus infection on natural killer cell development following hematopoietic stem cell transplant
    The American Association of Immunologists ; 2019
    In:  The Journal of Immunology Vol. 202, No. 1_Supplement ( 2019-05-01), p. 69.36-69.36
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 202, No. 1_Supplement ( 2019-05-01), p. 69.36-69.36
    Abstract: Hematopoietic stem cell transplant (HSCT) is a treatment for patients with hematological malignancies who are not eligible to receive intensive cytoreductive therapy. Cytomegalovirus (CMV) is an extremely prevalent infection and in immune-compromised patients, it is a significant cause of morbidity and mortality. Approximately two-thirds of seropositive patients experience CMV reactivation following HSCT. There have been reports that CMV reactivation causes increased activation of NK cells which actually benefits graft-versus-tumor effects. Our study objective is to delineate the kinetics of this effect and determine whether there are long-term functional differences in NK cells. We hypothesized that immune reconstitution is impacted by CMV infection and that the lymphopenic and inflammatory environment post-HSCT detrimentally affects the immune response to CMV infection. Using a syngeneic HSCT model in C57BL/6 mice, we studied de novo NK cell repopulation. At day 8 post-transplant, mice were inoculated with a low dose of mouse CMV. We found a significantly higher viral burden in the HSCT recipients compared to control mice. We found that CMV-specific NK cells (Ly49H+) rapidly expanded following CMV infection post-HSCT, but experienced a population collapse after two weeks. This is possibly due to exposure to a primary virus infection early on in development and/or the increased viral burden. There was a higher frequency of mature NK cells and IFN-gamma producing NK cells following CMV infection in the HSCT environment, suggestive of increased activation and accelerated differentiation. The disproportionate loss of the Ly49H+ NK cells may cause long-term functional defects in the HSCT recipient immune response.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.202.Supp.69.36
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2019
    detail.hit.zdb_id: 1475085-5
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  • 3
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    Online Resource
    Adiposity augments toxicity of mouse cytomegalovirus
    The American Association of Immunologists ; 2019
    In:  The Journal of Immunology Vol. 202, No. 1_Supplement ( 2019-05-01), p. 197.12-197.12
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 202, No. 1_Supplement ( 2019-05-01), p. 197.12-197.12
    Abstract: Obesity, a meta-inflammatory state defined by BMI≥30kg/m2, is reaching pandemic proportions. Generally, the impact of obesity on immune responses is poorly understood. Obesity is associated with chronic low-grade systemic pro-inflammatory cytokines. Similar to aging, obesity can affect immune responses and cause susceptibility to infection and pathology. Cytomegalovirus (CMV) is a prevalent herpes virus that can remain asymptomatic for years but causes significant morbidity and mortality in immunosuppressed patients. Our goal was to evaluate the impact of obesity on immune responses to CMV infection with a focus on toxicity. We reported that systemic immunotherapy results in elevated levels of pro-inflammatory cytokines in obese mice, leading to TNF-mediated pathological responses and death. We hypothesized that obesity will augment toxicity in mouse CMV (MCMV) infection as a consequence of heightened pro-inflammatory cytokine production. C57BL/6 and Balb/c were fed either a 60% fat (DIO) or 10% fat (Control) diet starting at 6-weeks old until 6-months old. DIO mice had significantly more subcutaneous and visceral adipose tissue than control mice assessed by MRI. Although ob/ob mice were fed a regular diet, they were significantly fatter than WT mice. Mice (DIO vs control and ob/ob vs WT) infected with 1–5×104 p.f.u. MCMV were assessed for clinical symptoms, serum cytokines, and survival. We observed that 50% of both DIO and ob/ob mice succumbed starting 2 days post-infection, which was associated with increased pro-inflammatory cytokine production. The augmented toxicity induced by MCMV in obese models demonstrates that adiposity is a critical factor in immune-mediated pathological responses to infections.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.202.Supp.197.12
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2019
    detail.hit.zdb_id: 1475085-5
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  • 4
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    Single cell and genomic profiling of PBMC-expanded NK cells in first-in-dog clinical trial of allogeneic adoptive NK cell therapy for dogs with cancer
    The American Association of Immunologists ; 2023
    In:  The Journal of Immunology Vol. 210, No. 1_Supplement ( 2023-05-01), p. 224.05-224.05
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 210, No. 1_Supplement ( 2023-05-01), p. 224.05-224.05
    Abstract: Natural killer (NK) cells are innate cytotoxic cells with a crucial role in anti-tumor responses, making them a promising candidate for adoptive immunotherapy (IT). CD5 depletion was previously used to isolate CD5 dim-expressing NK cells as a source of expanded NK cells for IT, but this technique can limit the yield of the final NK product. Here, we used bulk and single cell (SC) sequencing to compare ex vivo culture conditions using standard CD5 depletion versus unmanipulated PBMCs as the source of expanded NK cells comparing transcriptomic profiles from 5 matched healthy beagle donors using both techniques and subsequently from 5 dogs with naturally occurring malignant melanoma who received allogeneic PBMC-expanded NK cells in a first-in-dog clinical trial. Notably, beagle-derived PBMC-expanded cells had upregulation of NK pathways related to activation and function compared to CD5 depleted cells, suggesting bulk PBMCs may yield a superior product. Clinically, there were no serious adverse events using PBMC-expanded allogeneic NK cells, and one dog survived 445 days post-treatment, suggesting possible clinical benefit. SC analysis of PBMCs from this dog before, during, and after treatment showed a robust NK cell population across timepoints with high expression of cytotoxicity-related genes, such as GZMB and NCR3, lasting 14 days post-NK transfer. SC data also suggested a previously uncharacterized concordance of NK and CD8 T cell gene expression profiles in canine peripheral blood. Overall, allogeneic NK transfer using PBMC-expanded NK cells appears promising in dogs with cancer, and pre-clinical and clinical data support the use of SC analysis as a valuable technique for biomarker identification and optimizing NK IT in dogs. This study was funded by the National Institutes of Health/National Cancer Institute grant U01 CA224166-01, the 3U01CA224166-02S1 and 5R03CA252793-02 grants, and the V Foundation Victory over Cancer through the Canter Laboratory. Student support was provided by the AVMA/AVMF 2nd Opportunity Summer Research Scholarship.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.210.Supp.224.05
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2023
    detail.hit.zdb_id: 1475085-5
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  • 5
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    Online Resource
    Systemic Cancer Immunostimulatory Therapies and Acute Viral Infection Induce Corticosteroid-Mediated Thymic Involution and Naïve T cell Output in Mice and Humans
    The American Association of Immunologists ; 2023
    In:  The Journal of Immunology Vol. 210, No. 1_Supplement ( 2023-05-01), p. 145.21-145.21
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 210, No. 1_Supplement ( 2023-05-01), p. 145.21-145.21
    Abstract: Thymic involution (TI) occurs with aging and during stress responses, decreasing naïve T cell output. Thymic progenitor apoptosis can occur directly by corticosteroids (CS) leading to transient involution followed by recovery. The effects of systemic immunotherapies (IT) used in cancer or immune stimulation via acute viral infection on the thymus has not been well-characterized and was the primary goal of this study. IT treatment of mice with high dose IL-2 (HD IL-2) or models of acute viral infection (mouse cytomegalovirus, MCMV) all resulted in rapid TI due to apoptosis of CD4/CD8 double-positive progenitors followed with a reduction in naïve T cell content. Interestingly, cessation of therapy or resolution of viral infection resulted in greater thymic size compared to untreated recipients, indicating a rebound effect. In both models, increased CS levels in the serum of mice preceded TI. Clinically, patients receiving HD IL-2 for cancer had significantly reduced T cell receptor excision circles, a marker for naïve T cell output, also correlating with increased cortisol levels. Using a model of sub-lethal MCMV infection that did not increase systemic pro-inflammatory cytokines, we observed a similar correlation of TI and increased CS levels. To further analyze the effects of CS on TI, mice were adrenalectomized and then given HD IL-2, where significantly reduced CS levels correlated with partial protection from TI. These results indicate that strong systemic immunostimulation by either IT or acute viral infections markedly induce transient CS-mediated TI, leading to a decrease in naïve T cells. Therefore, targeting CS responses in preventing TI and, especially with the aged, allow for naïve T cell populations to be maintained.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.210.Supp.145.21
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2023
    detail.hit.zdb_id: 1475085-5
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  • 6
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    Online Resource
    Characterization of the Tumor Immune Microenvironment in Soft Tissue Sarcoma Patients Undergoing Surgery
    The American Association of Immunologists ; 2022
    In:  The Journal of Immunology Vol. 208, No. 1_Supplement ( 2022-05-01), p. 62.05-62.05
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 208, No. 1_Supplement ( 2022-05-01), p. 62.05-62.05
    Abstract: Tumor infiltrating lymphocytes (TILs) have been shown to predict survival in soft tissue sarcomas (STS), but the specific contribution of natural killer (NK) and CD8+ T cells to outcomes is undefined. Therefore, we sought to characterize the extent of NK and CD8+ T cell infiltration in STS. Prospectively, we evaluated 15 patients using fresh tumor from surgery for flow cytometric analysis. Retrospectively, we evaluated archived tumor tissue from 90 STS patients by immunohistochemistry (IHC) for CD3, CD8, CD45RO, NKp46, TIGIT, MHC-I, and p53. We analyzed metastasis-free survival (MFS) and overall survival (OS) by Kaplan-Meier method and log-rank test. By flow cytometry, we observed significant variability in CD45+ leukocytes in the STS TME (mean 29±24% of total live cells) with low percentages of tumor-infiltrating CD3-CD56+ NK cells (1.7±1.9% of total live cells and 5.3±3.0% of live CD45+ cells) and CD8+ T cells (1.6±1.6% of total live cells and 29.6±30.5% of live CD45+ cells). By IHC, NK and T cell infiltrates were low (median H score 0, range 0–66.5 and 2.7, range 0–110, respectively). We confirmed a positive correlation between CD8+ T cell infiltration and significantly improved OS (P & lt;0.05) and a trend for improved MFS. We also observed a trend for improved OS among patients with higher NKp46 scores (P=0.07). MHC-I expression positively correlated with both T and NK cell infiltration (P & lt;0.05), whereas TIGIT expression positively correlated with T cell infiltration (P & lt;0.05), but not NK infiltration. Infiltration of NK and CD8+ T cells is overall low in STS patients undergoing surgery but associated with superior OS. Further characterization of the immune infiltrate in STS may yield better biomarkers of prognosis and immune targeting. Supported by the following grants: NIH/NCI 1R03CA252793 NIH/NCI T32 CA251007-01
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.208.Supp.62.05
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2022
    detail.hit.zdb_id: 1475085-5
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  • 7
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    Online Resource
    IL-2 and Anti-TGF-β Promote NK Cell Reconstitution and Anti-tumor Effects after Syngeneic Hematopoietic Stem Cell Transplantation
    MDPI AG ; 2020
    In:  Cancers Vol. 12, No. 11 ( 2020-10-29), p. 3189-
    Details
    In: Cancers, MDPI AG, Vol. 12, No. 11 ( 2020-10-29), p. 3189-
    Abstract: The failure of autologous hematopoietic stem cell transplantation (HSCT) has been associated with a profound immunodeficiency that follows shortly after treatment, which renders patients susceptible to opportunistic infections and/or cancer relapse. Thus, given the additional immunosuppressive pathways involved in immune evasion in cancer, strategies that induce a faster reconstitution of key immune effector cells are needed. Natural killer (NK) cells mediate potent anti-tumor effector functions and are the first immune cells to repopulate after HSCT. TGF-β is a potent immunosuppressive cytokine that can impede both the development and function of immune cells. Here, we evaluated the use of an immunotherapeutic regimen that combines low dose of IL-2, an NK cell stimulatory signal, with TGF-β neutralization, in order to accelerate NK cell reconstitution following congenic HSCT in mice by providing stimulatory signals yet also abrogating inhibitory ones. This therapy led to a marked expansion of NK cells and accelerated NK cell maturation. Following HSCT, mature NK cells from the treated recipients displayed an activated phenotype and enhanced anti-tumor responses both in vitro and in vivo. No overt toxicities or adverse effects were observed in the treated recipients. However, these stimulatory effects on NK cell recovery were predicated upon continuous treatment as cessation of treatment led to return to baseline levels and to no improvement of overall immune recovery when assessed at later time-points, indicating strict regulatory control of the NK cell compartment. Overall, this study still demonstrates that therapies that combine positive and negative signals can be plausible strategies to accelerate NK cell reconstitution following HSCT and augment anti-tumor efficacy.
    Type of Medium: Online Resource
    ISSN: 2072-6694
    URL: Article
    DOI: 10.3390/cancers12113189
    Language: English
    Publisher: MDPI AG
    Publication Date: 2020
    detail.hit.zdb_id: 2527080-1
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  • 8
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    Online Resource
    Optimization of expansion techniques for adoptive NK cell transfer in dogs with cancer
    The American Association of Immunologists ; 2022
    In:  The Journal of Immunology Vol. 208, No. 1_Supplement ( 2022-05-01), p. 124.02-124.02
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 208, No. 1_Supplement ( 2022-05-01), p. 124.02-124.02
    Abstract: Natural killer (NK) cells can recognize heterogeneous cancer cell targets without prior sensitization, making them promising prospects for use in immunotherapy. We have completed first-in-dog feasibility clinical trials in dogs with cancer using both autologous and allogeneic NK cells expanded from peripheral blood mononuclear cells (PBMCs). Previously, CD5 depletion of PBMCs has been used to enrich for a CD5dim expressing subset prior to NK co-culture with an irradiated feeder line, but this can limit the yield of the final NK product. The purpose of this study was to compare ex vivo culture conditions using standard CD5 depletion versus unmanipulated PBMCs plus feeder line co-culture with 100 IU/mL rhIL-2 in matched healthy donors, hypothesizing that PBMCs plus feeder cells would generate an equivalent or superior NK product to CD5 depletion. Cell count, fold change, and viability data were collected for both techniques in 12 dogs across five time points up to day 14. A mixed-effects model analysis showed no statistical difference in calculated cell counts, overall fold change, and viability (p & gt;0.05 all) between PBMCs with feeders and CD5 depleted cells with feeders. PBMCs had a higher mean than CD5 depleted cells at day 14 in all three categories, reaching a peak mean of 677 million cells from 5 million PBMCs at day 0. Flow phenotype showed similar upregulation of NKp46 and Granzyme B expression. Killing assays against melanoma and osteosarcoma targets demonstrated comparable results among PBMCs plus feeders versus CD5 depleted NK cells (p & gt;0.05). Overall, these findings support the use of unmanipulated PBMCs plus feeder line coculture as an equivalent method to CD5 depletion in the expansion of canine NK cells for adoptive immunotherapy. Supported by grants from National Institutes of Health/National Cancer Institute (U01 CA224166-01, 1R03CA252793, T32 CA251007-01)
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.208.Supp.124.02
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2022
    detail.hit.zdb_id: 1475085-5
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  • 9
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    Online Resource
    Brain injury in COVID-19 is associated with dysregulated innate and adaptive immune responses
    Oxford University Press (OUP) ; 2022
    In:  Brain Vol. 145, No. 11 ( 2022-11-21), p. 4097-4107
    Details
    In: Brain, Oxford University Press (OUP), Vol. 145, No. 11 ( 2022-11-21), p. 4097-4107
    Abstract: COVID-19 is associated with neurological complications including stroke, delirium and encephalitis. Furthermore, a post-viral syndrome dominated by neuropsychiatric symptoms is common, and is seemingly unrelated to COVID-19 severity. The true frequency and underlying mechanisms of neurological injury are unknown, but exaggerated host inflammatory responses appear to be a key driver of COVID-19 severity. We investigated the dynamics of, and relationship between, serum markers of brain injury [neurofilament light (NfL), glial fibrillary acidic protein (GFAP) and total tau] and markers of dysregulated host response (autoantibody production and cytokine profiles) in 175 patients admitted with COVID-19 and 45 patients with influenza. During hospitalization, sera from patients with COVID-19 demonstrated elevations of NfL and GFAP in a severity-dependent manner, with evidence of ongoing active brain injury at follow-up 4 months later. These biomarkers were associated with elevations of pro-inflammatory cytokines and the presence of autoantibodies to a large number of different antigens. Autoantibodies were commonly seen against lung surfactant proteins but also brain proteins such as myelin associated glycoprotein. Commensurate findings were seen in the influenza cohort. A distinct process characterized by elevation of serum total tau was seen in patients at follow-up, which appeared to be independent of initial disease severity and was not associated with dysregulated immune responses unlike NfL and GFAP. These results demonstrate that brain injury is a common consequence of both COVID-19 and influenza, and is therefore likely to be a feature of severe viral infection more broadly. The brain injury occurs in the context of dysregulation of both innate and adaptive immune responses, with no single pathogenic mechanism clearly responsible.
    Type of Medium: Online Resource
    ISSN: 0006-8950 , 1460-2156
    URL: Article
    DOI: 10.1093/brain/awac321
    RVK:
    XA 10000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2022
    detail.hit.zdb_id: 1474117-9
    SSG: 12
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  • 10
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    Online Resource
    Obesity-Induced Microbiome Alterations Result in Severe Gastrointestinal Graft-Versus-Host Disease Following Allogeneic Hematopoietic Stem Cell Transplantation
    American Society of Hematology ; 2019
    In:  Blood Vol. 134, No. Supplement_1 ( 2019-11-13), p. 1922-1922
    Details
    In: Blood, American Society of Hematology, Vol. 134, No. Supplement_1 ( 2019-11-13), p. 1922-1922
    Abstract: Allogeneic hematopoietic stem cell transplantation (allo-HSCT) remains a viable treatment option for many cancers but its clinical utility is limited due to the occurrence of graft-versus-host disease (GVHD). Understanding the impact of obesity on immune function has become increasingly important in the setting of the current obesity pandemic. We report here that obesity has a negative and selective impact on acute gut GVHD. Diet-induced obese (DIO) mice exhibited increased gut permeability, endotoxin translocation and radiation-induced gastrointestinal damage. After allo-HSCT, DIO recipients across strains and sex had markedly increased pro-inflammatory cytokines (IL-6, TNF), GVHD biomarker ST2, MHC class II expression and exhibited rapid mortality associated with severe acute gut pathology. This obesity-associated lethal acute gut GVHD was dependent on donor CD4 T cells and occurred even in minor MHC mismatch strain combination in which only a delayed skin chronic GVHD resulted in lean recipients. Pro-inflammatory cytokine blockade targeting both IL-6 and TNF ameliorated obesity-associated acute gut GVHD while maintaining graft-versus-tumor (GVT) effects. Microbiome assessment of DIO mice revealed markedly reduced microbiome diversity and decreased Clostridiaceae abundance. Additionally, DIO mice had a significant increase of GVHD-associated Akkermansia muciniphila before and after allo-HSCT compared to the controls. Extended antibiotic treatment of DIO mice protected from the endotoxin translocation, cytokine storm as well as gut GVHD pathology but did not protect later development of chronic skin GVHD. These results demonstrate that obesity alters the microbiome and imparts differential effects on GVHD following allo-HSCT with decreased survival and this inferior outcome can be pre-empted by combined pro-inflammatory cytokine blockade or antibiotic pretreatment. Disclosures Pai: Roche-Genentech: Employment. Holtan:CSL Behring: Consultancy; Incyte: Consultancy; Bristol-Myers Squibb: Consultancy; Janssen: Consultancy. Ferrara:ViraCor: Consultancy; Incyte: Consultancy; Kamada: Consultancy; Mallinckrodt: Consultancy; Enlivex: Consultancy; Xenikos: Consultancy; CSL Behring: Consultancy; National Institutes of Health: Research Funding. Levine:Novartis: Honoraria; Kamada: Research Funding; bluebird bio: Consultancy; National Cancer Institute: Research Funding; Incyte: Consultancy, Research Funding; Ironwood: Honoraria; Biogen: Other: non-financial support; Viracor: Patents & Royalties: biomarker patent. Abedi:Abbie: Speakers Bureau; Gilead: Speakers Bureau; Celgene: Speakers Bureau; BMS: Speakers Bureau; Takeda: Speakers Bureau. Blazar:Kamon Pharmaceuticals, Inc: Membership on an entity's Board of Directors or advisory committees; Five Prime Therapeutics Inc: Co-Founder, Membership on an entity's Board of Directors or advisory committees; Regeneron Pharmaceuticals: Membership on an entity's Board of Directors or advisory committees; Magenta Therapeutics and BlueRock Therapeuetics: Membership on an entity's Board of Directors or advisory committees; Fate Therapeutics, Inc.: Research Funding; RXi Pharmaceuticals: Research Funding; Alpine Immune Sciences, Inc.: Research Funding; Abbvie Inc: Research Funding; Leukemia and Lymphoma Society: Research Funding; Childrens' Cancer Research Fund: Research Funding; KidsFirst Fund: Research Funding; Tmunity: Other: Co-Founder; BlueRock Therapeutics: Membership on an entity's Board of Directors or advisory committees.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood-2019-127743
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2019
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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