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  1 / 3355 MEDLINE  
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PMID:28747346
Autor:Nagalingam G; Vinuesa CG; Britton WJ; Saunders BM
Dirección:Tuberculosis Research Program, Centenary Institute, Newtown, New South Wales 2042, Australia.
Título:Modulation of Roquin Function in Myeloid Cells Reduces -Induced Inflammation.
Fuente:J Immunol; 199(5):1796-1804, 2017 09 01.
ISSN:1550-6606
País de publicación:United States
Idioma:eng
Resumen:Damaging inflammation is a hallmark of infection, and understanding how this is regulated is important for the development of new therapies to limit excessive inflammation. The E3 ubiquitin ligase, Roquin, is involved in immune regulation; however, its role in immunity to is unknown. To address this, we infected mice with a point mutation in ( ). Aerosol-infected mice showed enhanced control of infection associated with delayed bacterial dissemination and upregulated TNF production in the lungs after 2 wk. However, this early control of infection was not maintained, and by 8 wk postinfection mice demonstrated an increased bacterial burden and dysregulated inflammation in the lungs. As the inflammation in the lungs of the mice could have been influenced by emerging autoimmune conditions that are characteristic of the mice aging, the function of Roquin was examined in immune cell subsets in the absence of autoimmune complications. bacillus Calmette-Guérin-primed T cells transferred into mice provided equivalent protection in the spleen and liver. Interestingly, the transfer of mycobacteria-specific (P25 CD4 TCR transgenic) wild-type spleen cells into mice actually led to enhanced protection with reduced bacterial load, decreased chemokine expression, and reduced inflammation in the lungs compared with transfers into mice expressing intact Roquin. These studies suggest that modulation of Roquin in myeloid cells may reduce both inflammation and bacterial growth during the chronic phase of infection.
Tipo de publicación:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
Nombre de substancia:0 (Tumor Necrosis Factor-alpha); EC 2.3.2.27 (Rc3h1 protein, mouse); EC 2.3.2.27 (Ubiquitin-Protein Ligases)


  2 / 3355 MEDLINE  
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PMID:29205259
Autor:Mainardi C; Ebinger M; Enkel S; Feuchtinger T; Teltschik HM; Eyrich M; Schumm M; Rabsteyn A; Schlegel P; Seitz C; Schwarze CP; Müller I; Greil J; Bader P; Schlegel PG; Martin D; Holzer U; Döring M; Handgretinger R; Lang P
Dirección:Department of Paediatric Oncology, Children's University Hospital, University of Padova, Padova, Italy.
Título:CD34 selected stem cell boosts can improve poor graft function after paediatric allogeneic stem cell transplantation.
Fuente:Br J Haematol; 180(1):90-99, 2018 01.
ISSN:1365-2141
País de publicación:England
Idioma:eng
Resumen:Poor graft function (PGF) is a severe complication of haematopoietic stem cell transplantation (HSCT) and administration of donor stem cell boosts (SCBs) represents a therapeutic option. We report 50 paediatric patients with PGF who received 61 boosts with CD34 selected peripheral blood stem cells (PBSC) after transplantation from matched unrelated (n = 25) or mismatched related (n = 25) donors. Within 8 weeks, a significant increase in median neutrophil counts (0·6 vs. 1·516 × 10 /l, P < 0·05) and a decrease in red blood cell and platelet transfusion requirement (median frequencies 1 and 7 vs. 0, P < 0·0001 and <0·001), were observed, and 78·8% of patients resolved one or two of their cytopenias. 36·5% had a complete haematological response. Median lymphocyte counts for CD3 , CD3 CD4 , CD19 and CD56 increased 8·3-, 14·2-, 22.- and 1·6-fold. The rate of de novo acute graft-versus-host disease (GvHD) grade I-III was only 6% and resolved completely. No GvHD grade IV or chronic GvHD occurred. Patients who responded to SCB displayed a trend toward better overall survival (OS) (P = 0·07). Thus, administration of CD34 selected SCBs from alternative donors is safe and effective. Further studies are warranted to clarify the impact on immune reconstitution and survival.
Tipo de publicación:JOURNAL ARTICLE
Nombre de substancia:0 (Antigens, CD34)


  3 / 3355 MEDLINE  
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PMID:28457419
Autor:Clemente I; Goncalo A; Faria C; Dias M; Barbosa I; Mendes C
Dirección:Cancer Genetics Group, IPO-Porto Research Center (CI-IPOP), Portuguese Oncology Institute of Porto (IPO-Porto), Porto, Portugal.
Título:Relevance of Chimerism Analysis After Allogeneic Stem Cell Transplantation.
Fuente:Transplant Proc; 49(4):890-892, 2017 May.
ISSN:1873-2623
País de publicación:United States
Idioma:eng
Resumen:Hematopoietic stem cell transplantation is a potentially curative therapy for a range of malignant and non-malignant hematological diseases. Analysis of chimerism following allogeneic stem cell transplantation has been a routine method for the assessment of engraftment and early detection of graft failure. Lineage-specific chimerism monitoring is progressively used to specifically detect chimerism in one or more cell subsets, which may be undetected in assessment of the whole leukocyte population. The chimerism study in different leukocyte subpopulations increases sensitivity and specificity in the monitoring after transplantation, especially the analysis of T lymphocytes. All peripheral blood samples were separated into mononuclear cells and granulocytes by Ficoll density gradient centrifugation and T, B, and CD34+ was separated by immunomagnetic automatic cell separator. After DNA extraction, chimerism monitoring was performed using short tandem repeat by multiplex polymerase chain reaction followed by capillary electrophoresis. Quantification of chimerism was performed by determining the ratio of peak areas from donor and recipient informative short tandem repeat. Donor-recipient chimerism analysis in patients after allogeneic stem cell transplantation is a practical, feasible, and useful tool that predicts clinical outcomes and provides a guide for suitable therapeutic interventions.
Tipo de publicación:JOURNAL ARTICLE


  4 / 3355 MEDLINE  
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PMID:28887325
Autor:Fitzhugh CD; Cordes S; Taylor T; Coles W; Roskom K; Link M; Hsieh MM; Tisdale JF
Dirección:Sickle Cell Branch, National Heart, Lung, and Blood Institute (NHLBI).
Título:At least 20% donor myeloid chimerism is necessary to reverse the sickle phenotype after allogeneic HSCT.
Fuente:Blood; 130(17):1946-1948, 2017 Oct 26.
ISSN:1528-0020
País de publicación:United States
Idioma:eng
Resumen:Novel curative therapies using genetic transfer of normal globin-producing genes into autologous hematopoietic stem cells (HSCs) are in clinical trials for patients with sickle cell disease (SCD). The percentage of transferred globin necessary to cure SCD is currently not known. In the setting of allogeneic nonmyeloablative HSC transplants (HSCTs), stable mixed chimerism is sufficient to reverse the disease. We regularly monitored 67 patients after HSCT. After initially robust engraftment, 3 of these patients experienced declining donor myeloid chimerism (DMC) levels with eventual return of disease. From this we discovered that 20% DMC is necessary to reverse the sickle phenotype. We subsequently developed a mathematical model to test the hypothesis that the percentage of DMC necessary is determined solely by differences between donor and recipient red blood cell (RBC) survival times. In our model, the required 20% DMC can be entirely explained by the large differences between donor and recipient RBC survival times. Our model predicts that the requisite DMC and therefore necessary level of transferred globin is lowest in patients with the highest reticulocyte counts and concomitantly shortened RBC lifespans.
Tipo de publicación:JOURNAL ARTICLE
Nombre de substancia:0 (Hemoglobin, Sickle)


  5 / 3355 MEDLINE  
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PMID:28859032
Autor:Thakkar D; Katewa S; Rastogi N; Kohli S; Nivargi S; Yadav SP
Dirección:Pediatric Hematology Oncology and Bone Marrow Transplant Unit, Department of Pediatrics, Fortis Memorial Research Institute, Gurgaon, Haryana, India.
Título:Successful Reduced Intensity Conditioning Alternate Donor Stem Cell Transplant for Wiskott-Aldrich Syndrome.
Fuente:J Pediatr Hematol Oncol; 39(8):e493-e496, 2017 Nov.
ISSN:1536-3678
País de publicación:United States
Idioma:eng
Resumen:There are very few reports of reduced intensity conditioning (RIC) hematopoietic stem cell transplant (HSCT) with alternate donor for Wiskott-Aldrich syndrome (WAS) and there is no report of RIC with posttransplant cyclophosphamide (PTCy) in WAS. There is only 1 report of T cell receptor αß and CD19-depleted haploidentical HSCT for WAS. Here we report successful outcome in 3 children with WAS who underwent successful RIC alternate donor HSCT of whom 2 (matched unrelated donor and T-cell replete haploidentical) received PTCy and 1 underwent T cell receptor αß and CD19-depleted haploidentical HSCT. We modified conditioning used by Luznik for haploidentical HSCT by adding thiotepa 8 mg/kg and Campath or rabbit antithymoglobulin for 2 cases who received PTCy. In third case we gave fludarabine, thiotepa, and treosulfan-based conditioning. The mean duration of follow-up for these patients was 23.6 months posttransplant (range, 21 to 26 mo). All 3 patients are transfusion independent. Acute graft versus host disease (GVHD) grade I occurred in 1 and none had chronic GVHD. Chimerism of all 3 was fully donor (>95% donor) at D+30 and D+100 posttransplant. All are alive, healthy, and doing well. Our 3 cases highlight that with newer conditioning and GVHD prophylaxis approach alternate donor HSCT in WAS can become a safe and effective treatment option.
Tipo de publicación:CASE REPORTS; JOURNAL ARTICLE


  6 / 3355 MEDLINE  
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PMID:28834486
Autor:Abramson JS; McGree B; Noyes S; Plummer S; Wong C; Chen YB; Palmer E; Albertson T; Ferry JA; Arrillaga-Romany IC
Dirección:Massachusetts General Hospital Cancer Center, Boston, MA jabramson@mgh.harvard.edu.
Título:Anti-CD19 CAR T Cells in CNS Diffuse Large-B-Cell Lymphoma.
Fuente:N Engl J Med; 377(8):783-784, 2017 08 24.
ISSN:1533-4406
País de publicación:United States
Idioma:eng
Tipo de publicación:CASE REPORTS; LETTER
Nombre de substancia:0 (Antigens, CD19); 0 (Antineoplastic Agents); 0 (Receptors, Antigen, T-Cell)


  7 / 3355 MEDLINE  
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PMID:28754799
Autor:Llewellyn RA; Thomas KS; Gutknecht MF; Bouton AH
Dirección:Department of Microbiology, Immunology, and Cancer Biology, University of Virginia School of Medicine, Charlottesville, Virginia, USA.
Título:The nonreceptor protein tyrosine kinase Pyk2 promotes the turnover of monocytes at steady state.
Fuente:J Leukoc Biol; 102(4):1069-1080, 2017 Oct.
ISSN:1938-3673
País de publicación:United States
Idioma:eng
Resumen:Monocytes are short-lived myeloid cells that perform functions essential for tissue homeostasis and disease resolution. However, the cellular mechanisms controlling the maintenance and turnover of monocyte populations are largely undefined. Proline-rich tyrosine kinase 2 (Pyk2) is a nonreceptor tyrosine kinase that regulates numerous immune cell functions, but its role in monocytes is currently unknown. In this study, we sought to characterize the expression and function of Pyk2 in lineage-committed monocyte populations. Here, we report that Pyk2 protein expression is increased in the Ly6C monocyte population. Using a Pyk2 knockout mouse model (Pyk2 ), we show that Pyk2 regulates the relative proportion of monocyte subsets normally represented in the bone marrow (BM) at steady state. In support of this conclusion, a similar phenotype was observed in the peripheral blood and spleen. Data from reciprocal BM chimera experiments indicate that the alterations in monocyte populations exhibited by Pyk2 mice are due to factors intrinsic to the monocytes. Lineage-tracing of monocyte populations suggests that Pyk2 promotes apoptosis in BM monocytes, thereby acting as an important homeostatic regulator of turnover in these short-lived, innate immune cells.
Tipo de publicación:JOURNAL ARTICLE
Nombre de substancia:EC 2.7.10.2 (Focal Adhesion Kinase 2); EC 2.7.10.2 (Ptk2b protein, mouse)


  8 / 3355 MEDLINE  
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PMID:28720651
Autor:Masaki H; Nakauchi H
Dirección:Center for Stem Cell Biology and Regenerative Medicine, Institute of Medical Science, University of Tokyo, Tokyo 108-8639, Japan.
Título:Interspecies chimeras for human stem cell research.
Fuente:Development; 144(14):2544-2547, 2017 07 15.
ISSN:1477-9129
País de publicación:England
Idioma:eng
Resumen:Interspecies chimeric assays are a valuable tool for investigating the potential of human stem and progenitor cells, as well as their differentiated progeny. This Spotlight article discusses the different factors that affect interspecies chimera generation, such as evolutionary distance, developmental timing, and apoptosis of the transplanted cells, and suggests some possible strategies to address them. A refined approach to generating interspecies chimeras could contribute not only to a better understanding of cellular potential, but also to understanding the nature of xenogeneic barriers and mechanisms of heterochronicity, to modeling human development, and to the creation of human transplantable organs.
Tipo de publicación:JOURNAL ARTICLE


  9 / 3355 MEDLINE  
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PMID:28667356
Autor:Candéias SM; Mika J; Finnon P; Verbiest T; Finnon R; Brown N; Bouffler S; Polanska J; Badie C
Dirección:CEA, Fundamental Research Division, Biosciences and Biotechnologies Institute, Laboratory of Chemistry and Biology of Metals, 38054, Grenoble, France. serge.candeias@cea.fr.
Título:Low-dose radiation accelerates aging of the T-cell receptor repertoire in CBA/Ca mice.
Fuente:Cell Mol Life Sci; 74(23):4339-4351, 2017 Dec.
ISSN:1420-9071
País de publicación:Switzerland
Idioma:eng
Resumen:While the biological effects of high-dose-ionizing radiation on human health are well characterized, the consequences of low-dose radiation exposure remain poorly defined, even though they are of major importance for radiological protection. Lymphocytes are very radiosensitive, and radiation-induced health effects may result from immune cell loss and/or immune system impairment. To decipher the mechanisms of effects of low doses, we analyzed the modulation of the T-cell receptor gene repertoire in mice exposed to a single low (0.1 Gy) or high (1 Gy) dose of radiation. High-throughput T-cell receptor gene profiling was used to visualize T-lymphocyte dynamics over time in control and irradiated mice. Radiation exposure induces "aging-like" effects on the T-cell receptor gene repertoire, detectable as early as 1 month post-exposure and for at least 6 months. Surprisingly, these effects are more pronounced in animals exposed to 0.1 Gy than to 1 Gy, where partial correction occurs over time. Importantly, we found that low-dose radiation effects are partially due to the hematopoietic stem cell impairment. Collectively, our findings show that acute low-dose radiation exposure specifically results in long-term alterations of the T-lymphocyte repertoire.
Tipo de publicación:JOURNAL ARTICLE
Nombre de substancia:0 (Protein Isoforms); 0 (Receptors, Antigen, T-Cell)


  10 / 3355 MEDLINE  
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PMID:28632753
Autor:Shaler CR; Choi J; Rudak PT; Memarnejadian A; Szabo PA; Tun-Abraham ME; Rossjohn J; Corbett AJ; McCluskey J; McCormick JK; Lantz O; Hernandez-Alejandro R; Haeryfar SMM
Dirección:Department of Microbiology and Immunology, Western University, London, Ontario, Canada.
Título:MAIT cells launch a rapid, robust and distinct hyperinflammatory response to bacterial superantigens and quickly acquire an anergic phenotype that impedes their cognate antimicrobial function: Defining a novel mechanism of superantigen-induced immunopathology and immunosuppression.
Fuente:PLoS Biol; 15(6):e2001930, 2017 Jun.
ISSN:1545-7885
País de publicación:United States
Idioma:eng
Resumen:Superantigens (SAgs) are potent exotoxins secreted by Staphylococcus aureus and Streptococcus pyogenes. They target a large fraction of T cell pools to set in motion a "cytokine storm" with severe and sometimes life-threatening consequences typically encountered in toxic shock syndrome (TSS). Given the rapidity with which TSS develops, designing timely and truly targeted therapies for this syndrome requires identification of key mediators of the cytokine storm's initial wave. Equally important, early host responses to SAgs can be accompanied or followed by a state of immunosuppression, which in turn jeopardizes the host's ability to combat and clear infections. Unlike in mouse models, the mechanisms underlying SAg-associated immunosuppression in humans are ill-defined. In this work, we have identified a population of innate-like T cells, called mucosa-associated invariant T (MAIT) cells, as the most powerful source of pro-inflammatory cytokines after exposure to SAgs. We have utilized primary human peripheral blood and hepatic mononuclear cells, mouse MAIT hybridoma lines, HLA-DR4-transgenic mice, MAIThighHLA-DR4+ bone marrow chimeras, and humanized NOD-scid IL-2Rγnull mice to demonstrate for the first time that: i) mouse and human MAIT cells are hyperresponsive to SAgs, typified by staphylococcal enterotoxin B (SEB); ii) the human MAIT cell response to SEB is rapid and far greater in magnitude than that launched by unfractionated conventional T, invariant natural killer T (iNKT) or γδ T cells, and is characterized by production of interferon (IFN)-γ, tumor necrosis factor (TNF)-α and interleukin (IL)-2, but not IL-17A; iii) high-affinity MHC class II interaction with SAgs, but not MHC-related protein 1 (MR1) participation, is required for MAIT cell activation; iv) MAIT cell responses to SEB can occur in a T cell receptor (TCR) Vß-specific manner but are largely contributed by IL-12 and IL-18; v) as MAIT cells are primed by SAgs, they also begin to develop a molecular signature consistent with exhaustion and failure to participate in antimicrobial defense. Accordingly, they upregulate lymphocyte-activation gene 3 (LAG-3), T cell immunoglobulin and mucin-3 (TIM-3), and/or programmed cell death-1 (PD-1), and acquire an anergic phenotype that interferes with their cognate function against Klebsiella pneumoniae and Escherichia coli; vi) MAIT cell hyperactivation and anergy co-utilize a signaling pathway that is governed by p38 and MEK1/2. Collectively, our findings demonstrate a pathogenic, rather than protective, role for MAIT cells during infection. Furthermore, we propose a novel mechanism of SAg-associated immunosuppression in humans. MAIT cells may therefore provide an attractive therapeutic target for the management of both early and late phases of severe SAg-mediated illnesses.
Tipo de publicación:COMPARATIVE STUDY; JOURNAL ARTICLE
Nombre de substancia:0 (Antigens, Bacterial); 0 (Enterotoxins); 0 (Superantigens); 39424-53-8 (enterotoxin B, staphylococcal)



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