Institution
Miltenyi Biotec
Company•Cologne, Germany•
About: Miltenyi Biotec is a company organization based out in Cologne, Germany. It is known for research contribution in the topics: Antigen & T cell. The organization has 539 authors who have published 638 publications receiving 36046 citations.
Topics: Antigen, T cell, Cytotoxic T cell, Immune system, Stem cell
Papers published on a yearly basis
Papers
More filters
••
Rockefeller University1, University of Basel2, Memorial Sloan Kettering Cancer Center3, Swiss Institute of Bioinformatics4, Sapienza University of Rome5, German Cancer Research Center6, Ludwig Maximilian University of Munich7, University of Freiburg8, Miltenyi Biotec9, J. Craig Venter Institute10, Columbia University11, University of Naples Federico II12, University of Düsseldorf13, University of Bonn14, Semmelweis University15, Yeshiva University16, National Institutes of Health17, Cornell University18
TL;DR: A relatively small set of miRNAs, many of which are ubiquitously expressed, account for most of the differences in miRNA profiles between cell lineages and tissues.
3,687 citations
••
University of Leicester1, Université de Montréal2, Burnet Institute3, French Institute of Health and Medical Research4, Centre national de la recherche scientifique5, University of Giessen6, Erasmus University Medical Center7, University of Texas MD Anderson Cancer Center8, University of Oxford9, Icahn School of Medicine at Mount Sinai10, Ludwig Maximilian University of Munich11, Miltenyi Biotec12, Walter and Eliza Hall Institute of Medical Research13, University of Brescia14, Jagiellonian University Medical College15, John Radcliffe Hospital16, University of Würzburg17
TL;DR: The present document proposes a nomenclature for monocytes and defines 3 types of monocytes (classical, intermediate, and nonclassical monocytes) and3 types of dendritic cells (plasmacytoid and 2 types of myeloid dendrites) in human and in mouse blood.
2,111 citations
••
TL;DR: The three presumably novel Ags serve as specific markers for the respective subpopulations of blood dendritic cells in fresh blood and will be of great value for their further analysis and to evaluate their therapeutic potential.
Abstract: We have generated a panel of mAbs that identify three presumably novel human dendritic cell Ags: BDCA-2, BDCA-3, and BDCA-4. In blood, BDCA-2 and BDCA-4 are expressed on CD11c− CD123bright plasmacytoid dendritic cells, whereas BDCA-3 is expressed on small population of CD11c+ CD123− dendritic cells. All three Ags are not detectable on a third blood dendritic cell population, which is CD1c+ CD11cbright CD123dim, or on any other cells in blood. BDCA-4 is also expressed on monocyte-derived and CD34+ cell-derived dendritic cells. Expression of all three Ags dramatically changes once blood dendritic cells undergo in vitro maturation. BDCA-2 is completely down-regulated on plasmacytoid CD11c− CD123bright dendritic cells, expression of BDCA-3 is up-regulated on both plasmacytoid CD11c− CD123bright dendritic cells and CD1c+ CD11cbright CD123dim dendritic cells, and expression of BDCA-4 is up-regulated on CD1c+ CD11cbright CD123dim dendritic cells. BDCA-2 is rapidly internalized at 37°C after mAb labeling. The three presumably novel Ags serve as specific markers for the respective subpopulations of blood dendritic cells in fresh blood and will be of great value for their further analysis and to evaluate their therapeutic potential.
1,356 citations
••
TL;DR: CD4 + T cells that are reactive against the spike glycoprotein of SARS-CoV-2 in the peripheral blood of patients with COVID-19 and healthy donors are found, indicating that spike-protein cross-reactive T cells are present and probably generated during previous encounters with endemic coronaviruses.
Abstract: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused the rapidly unfolding coronavirus disease 2019 (COVID-19) pandemic1,2. Clinical manifestations of COVID-19 vary, ranging from asymptomatic infection to respiratory failure. The mechanisms that determine such variable outcomes remain unresolved. Here we investigated CD4+ T cells that are reactive against the spike glycoprotein of SARS-CoV-2 in the peripheral blood of patients with COVID-19 and SARS-CoV-2-unexposed healthy donors. We detected spike-reactive CD4+ T cells not only in 83% of patients with COVID-19 but also in 35% of healthy donors. Spike-reactive CD4+ T cells in healthy donors were primarily active against C-terminal epitopes in the spike protein, which show a higher homology to spike glycoproteins of human endemic coronaviruses, compared with N-terminal epitopes. Spike-protein-reactive T cell lines generated from SARS-CoV-2-naive healthy donors responded similarly to the C-terminal region of the spike proteins of the human endemic coronaviruses 229E and OC43, as well as that of SARS-CoV-2. This results indicate that spike-protein cross-reactive T cells are present, which were probably generated during previous encounters with endemic coronaviruses. The effect of pre-existing SARS-CoV-2 cross-reactive T cells on clinical outcomes remains to be determined in larger cohorts. However, the presence of spike-protein cross-reactive T cells in a considerable fraction of the general population may affect the dynamics of the current pandemic, and has important implications for the design and analysis of upcoming trials investigating COVID-19 vaccines.
1,040 citations
••
TL;DR: Triggering of BDCA-2 should be evaluated as therapeutic strategy for blocking production of interferon alpha/beta in systemic lupus erythematosus patients.
Abstract: Plasmacytoid dendritic cells are present in lymphoid and nonlymphoid tissue and contribute substantially to both innate and adaptive immunity. Recently, we have described several monoclonal antibodies that recognize a plasmacytoid dendritic cell-specific antigen, which we have termed BDCA-2. Molecular cloning of BDCA-2 revealed that BDCA-2 is a novel type II C-type lectin, which shows 50.7% sequence identity at the amino acid level to its putative murine ortholog, the murine dendritic cell–associated C-type lectin 2. Anti–BDCA-2 monoclonal antibodies are rapidly internalized and efficiently presented to T cells, indicating that BDCA-2 could play a role in ligand internalization and presentation. Furthermore, ligation of BDCA-2 potently suppresses induction of interferon α/β production in plasmacytoid dendritic cells, presumably by a mechanism dependent on calcium mobilization and protein-tyrosine phosphorylation by src-family protein-tyrosine kinases. Inasmuch as production of interferon α/β by plasmacytoid dendritic cells is considered to be a major pathophysiological factor in systemic lupus erythematosus, triggering of BDCA-2 should be evaluated as therapeutic strategy for blocking production of interferon α/β in systemic lupus erythematosus patients.
811 citations
Authors
Showing all 541 results
Name | H-index | Papers | Citations |
---|---|---|---|
Kay Hofmann | 101 | 227 | 45723 |
Werner Müller | 89 | 292 | 37724 |
John M. Campbell | 54 | 119 | 11474 |
Wing Leung | 50 | 203 | 9704 |
Alexander Scheffold | 49 | 109 | 10083 |
Zhongyu Zhu | 35 | 118 | 4089 |
Andreas Bosio | 34 | 132 | 7563 |
Rimas J. Orentas | 33 | 94 | 7302 |
Sascha Rutz | 31 | 47 | 4952 |
Jürgen Schmitz | 28 | 49 | 5416 |
Boro Dropulic | 27 | 131 | 3727 |
Andreas Thiel | 27 | 80 | 4218 |
Christoph Coch | 25 | 59 | 2851 |
Mario Assenmacher | 25 | 47 | 3645 |
Dmytro A. Yushchenko | 22 | 60 | 1560 |