Daniel Pinschewer
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Professor at University of Basel
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About
Daniel Pinschewer is a Professor at the University of Basel in Switzerland. His research primarily focuses on immunology, particularly in the areas of T cell responses and vaccination mechanisms against viral infections. Recent work includes studies on the immune responses to Orf virus-based vectors, the impact of mRNA vaccination on germinal center reactions, and the role of IL-33 in regulating immune responses in chronic infections.
Recent Grants
Grant: Close
Correlates of protective immunity to SARS-Coronavirus 2
Open Date: 2020-10-01
Close Date: 2022-09-01
Grant: Close
EVA-GLOBAL: European Virus Archive goes global
Open Date: 2020-01-01
Close Date: 2023-12-01
Grant: Close
Alarmin’ for T cell self renewal
Open Date: 2019-04-01
Close Date: 2023-03-01
Grant: Close
VacPath: Novel vaccine vectors to resist pathogen challenge
Open Date: 2019-01-01
Close Date: 2022-12-01
Grant: Close
“Immunity and tolerance in persistent viral infection”
Open Date: 2017-04-01
Close Date: 2021-09-01
Articles (20)
Emergence and fate of stem cell–like <i>Tcf7</i> <sup>+</sup> CD8 <sup>+</sup> T cells during a primary immune response to viral infection
In response to infection, naïve CD8 + T (T N ) cells yield a large pool of short-lived terminal effector (T TE ) cells that eliminate infected host cells. In parallel, a minor population of stem cell–like central memory (T CM ) cells forms, which has the capacity to maintain immunity after pathogen clearance. It has remained uncertain whether stem-like T CM cells arise by dedifferentiation from a subset of cytolytic T TE cells or whether priming generates stem-like cells capable of seeding the T CM compartment and, if so, when cytolytic T TE cells branch off. Here, we show that CD8 + T cells with stem-like properties, which are identified by the expression of TCF1 (encoded by Tcf7 ), are present across the primary response to infection. Priming programs T N cells to undergo multiple cell divisions, over the course of which TCF1 expression is maintained. These TCF1 + cells further expand relatively independently of systemic inflammation, antigen dose, or affinity, and they quantitatively yield TCF1 + T CM cells after pathogen clearance. Inflammatory signals suppress TCF1 expression in early divided TCF1 + cells. TCF1 down-regulation is associated with the irreversible loss of self-renewal capacity and the silencing of stem/memory genes, which precedes the stable acquisition of a T TE state. TCF1 expression restrains cell cycling, explaining in part the limited expansion of TCF1 + relative to TCF1 − cells during the primary response. Thus, our data are consistent with terminal differentiation of effector cells being a step-wise process that is initiated by inflammation in primed stem-like cells, which would otherwise become central memory cells by default.
Year:
2023
Collaborators (12)
Sanjiv Luther
Full Professor
University of Lausanne
Werner Held
University of Lausanne
Doron Merkler
University of Geneva
Weng Ming Ng
University of Oxford
Thomas A. Bowden
University of Oxford
Christoph Dehio
University of Basel
Max Löhning
University Professor
Charité - Universitätsmedizin Berlin
Peter Reuther
Leibniz-Institut für Experimentelle Virologie
Florian Kreppel
Private Universität Witten/Herdecke gGmbH
Carolyn G. King
University Hospital Basel
Katie Doores
Senior Lecturer/MRC Career Development Fellow
King’s College London
Frederik Heinrich
Deutsches Rheuma-Forschungszentrum Berlin

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