Institution
University of Düsseldorf
Education•Düsseldorf, Germany•
About: University of Düsseldorf is a education organization based out in Düsseldorf, Germany. It is known for research contribution in the topics: Population & Transplantation. The organization has 25225 authors who have published 49155 publications receiving 1946434 citations.
Topics: Population, Transplantation, Diabetes mellitus, Gene, Type 2 diabetes
Papers published on a yearly basis
Papers
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TL;DR: Air pollution exposure was significantly correlated to extrinsic skin aging signs, in particular to pigment spots and less pronounced to wrinkles, indicating that particle pollution might influence skin aging as well.
354 citations
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TL;DR: Although both areas participate in verbal fluency, they do so differentially, and area 44 is probably involved in high-level aspects of programming speech production per se, which opens new perspectives for analyzing the cortical networks involved in language.
354 citations
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TL;DR: A molecular mechanism of in vivo vascular lumen formation in developing blood vessels is proposed and VE-Cadherin and VEGF-A act at different steps, required for localizing CD34-sialomucins to the endothelial cell-cell contact and EC shape change.
354 citations
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TL;DR: Insight is provided into the requirements for persistence of T cell immune responses in the face of exhaustion and mechanisms by which effective T cell–mediated immunity may be enhanced during chronic infections and cancer are suggested.
Abstract: During chronic viral infections and in cancer, T cells become dysfunctional, a state known as T cell exhaustion. Although it is well recognized that memory CD8 T cells account for the persistence of CD8 T cell immunity after acute infection, how exhausted T cells persist remains less clear. Using chronic infection with lymphocytic choriomeningitis virus clone 13 and tumor samples, we demonstrate that CD8 T cells differentiate into a less exhausted TCF1high and a more exhausted TCF1low population. Virus-specific TCF1high CD8 T cells, which resemble T follicular helper (TFH) cells, persist and recall better than do TCF1low cells and act as progenitor cells to replenish TCF1low cells. We show that TCF1 is both necessary and sufficient to support this progenitor-like CD8 subset, whereas cell-intrinsic type I interferon signaling suppresses their differentiation. Accordingly, cell-intrinsic TCF1 deficiency led to a loss of these progenitor CD8 T cells, sharp contraction of virus-specific T cells, and uncontrolled viremia. Mechanistically, TCF1 repressed several pro-exhaustion factors and induced Bcl6 in CD8 T cells, which promoted the progenitor fate. We propose that the TCF1-Bcl6 axis counteracts type I interferon to repress T cell exhaustion and maintain T cell stemness, which is critical for persistent antiviral CD8 T cell responses in chronic infection. These findings provide insight into the requirements for persistence of T cell immune responses in the face of exhaustion and suggest mechanisms by which effective T cell–mediated immunity may be enhanced during chronic infections and cancer.
353 citations
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TL;DR: CFF is a sensitive, simple, and reliable parameter for quantification of low‐grade HE severity in cirrhotic patients and may be useful for the detection and monitoring of SHE.
352 citations
Authors
Showing all 25575 results
Name | H-index | Papers | Citations |
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Karl J. Friston | 217 | 1267 | 217169 |
Roderick T. Bronson | 169 | 679 | 107702 |
Stanley B. Prusiner | 168 | 745 | 97528 |
Ralph A. DeFronzo | 160 | 759 | 132993 |
Monique M.B. Breteler | 159 | 546 | 93762 |
Thomas Meitinger | 155 | 716 | 108491 |
Karl Zilles | 138 | 692 | 72733 |
Ruben C. Gur | 136 | 741 | 61312 |
Alexis Brice | 135 | 870 | 83466 |
Michael Schmitt | 134 | 2007 | 114667 |
Michael Weller | 134 | 1105 | 91874 |
Helmut Sies | 133 | 670 | 78319 |
Peter T. Fox | 131 | 622 | 83369 |
Yuri S. Kivshar | 126 | 1845 | 79415 |
Markus M. Nöthen | 125 | 943 | 83156 |