Daniel Utzschneider is a Special Fellow of The Leukemia & Lymphoma Society. He completed his PhD in the group of Professor Dietmar Zehn at the University of Lausanne, Switzerland in 2014 before relocating to the University of California San Diego for his postdoctoral studies in Professor Stephen Hedrick’s laboratory. He then joined the research group of Professor Axel Kallies at the Doherty Institute in 2018. Daniel’s research focuses on CD8 T cell differentiation in chronic infection and cancer - a phenomenon most widely known as T cell exhaustion.
Daniel’s work has revealed crucial insights in the T cell differentiation in chronic infection including the discovery of a subpopulation of precursor exhausted T cells that are responsible for maintaining T cell responses in chronic infection and cancer as well as for the proliferative burst following checkpoint blockade, a widely applied immunotherapy for cancer patients. Daniel’s work has resulted in various first-author publications in leading journals such Nature Immunology, Immunity, the Journal of Experimental Medicine and Cell Reports and he has been awarded with the “Prix d’excellence“ from the University of Lausanne, Switzerland. In 2019, the Robert Koch Foundation (Germany) honoured him with a very prestigious award recognizing the next generation of scientists. Daniel has received multiple fellowships to support his work including an Early- and an Advanced Postdoc.Mobility fellowship from the Swiss National Science Foundation, a Career development program from the Leukemia & Lymphoma Society and an Emerging Leadership Investigator Grant (from 2021) as well as multiple research grants from the University of Melbourne.
CD8+ T cells persistently exposed to antigen, such as during chronic viral infections and in tumors, undergo substantial functional and phenotypic changes, a state widely known as T cell 'exhaustion'. This includes impairments in effector function and elevated expression of inhibitory receptors such as PD-1. Inhibitory receptors constitute critical checkpoints in T cell activation and their expression represents a major mechanism by which T cell proliferation and function are limited. Blocking the activity of PD-1 augments T cell mediated immunity and has revolutionized our approach to the treatment of many cancers. However, despite the unparalleled success of this so-called checkpoint blockade, it does not revert the functional impairments linked to T cell exhaustion, which constitutes a critical limitation in utilizing the full potential of the body's immune response.
Our group studies the mechanisms inducing T cell exhaustion with the ultimate goal to identify targets that can lead to the design and development of novel therapeutic treatments to improve health of patients suffering from chronic infections or cancer.
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