Persistent viral infections are characterized by the simultaneous presence of chronic inflammation and T cell dysfunction. In prototypic models of chronicity-infection with human immunodeficiency virus (HIV) or lymphocytic choriomeningitis virus (LCMV)-we used transcriptome-based modeling to reveal that CD4(+) T cells were co-exposed not only to multiple inhibitory signals but also to tumor-necrosis factor (TNF). Blockade of TNF during chronic infection with LCMV abrogated the inhibitory gene-expression signature in CD4(+) T cells, including reduced expression of the inhibitory receptor PD-1, and reconstituted virus-specific immunity, which led to control of infection. Preventing signaling via the TNF receptor selectively in T cells sufficed to induce these effects. Targeted immunological interventions to disrupt the TNF-mediated link between chronic inflammation and T cell dysfunction might therefore lead to therapies to overcome persistent viral infection.
Unit 1
Unit 1: Genetics, Developmental Biology & Molecular Physiology
- Margret Bülow lab: Neuronal Cell Metabolism
- Michael Hoch/Reinhard Bauer lab: Molecular Developmental Biology
- Elvira Mass lab: Developmental Biology of the Immune System
- Michael Pankratz lab: Molecular Brain Physiology and Behavior
- Dietmar Schmucker lab: Neuronal Wiring
- Peter Soba lab: Neuronal Patterning and Connectivity
Unit 2
Unit 2: Molecular Immune & Cell Biology
- Sven Burgdorf lab: Cellular Immunology
- Irmgard Förster lab: Immunology and Environment
- Jan Hasenauer lab: Computational Life Sciences
- Eva Kiermaier lab: Immune and Tumor Biology
- Waldemar Kolanus lab: Molecular Immunology and Cell Biology
- Mihai Netea lab: Immunology and Metabolism
- Joachim Schultze lab: Genomics and Immunoregulation
- Ivonne Vazquez Armendariz lab: Organoid Biology
- Andreas Schlitzer lab: Quantitative Systems Biology
Unit 3
Unit 4
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