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: Genetik, Entwicklungsbiologie & Molekulare Physiologie
- Margret Bülow: Zellstoffwechsel von Neuronen
- Michael Hoch/Reinhard Bauer: Entwicklungsgenetik & Molekulare Physiologie
- Elvira Mass: Entwicklungsbiologie des Immunsystems
- Michael Pankratz: Molekulare Hirnphysiologie & Verhaltensforschung
- Dietmar Schmucker: Entwicklung neuronaler Verschaltungen
- Peter Soba: Neuronale Musterbildung und Konnektivität
Unit 2
Unit 2: Molekulare Immun- & Zellbiologie
- Sven Burgdorf: Zelluläre Immunologie
- Irmgard Förster: Immunologie & Umwelt
- Jan Hasenauer: Rechnergestützte Lebenswissenschaften
- Eva Kiermaier: Immun- und Tumorbiologie
- Waldemar Kolanus: Molekulare Immunologie und Zellbiologie
- Mihai Netea: Immunologie und Metabolismus
- Joachim Schultze: Genomik & Immunregulation
- Ivonne Vazquez Armendariz: Organoide Biologie
- Andreas Schlitzer: Quantitative Systembiologie
Unit 3
Unit 4
Ehemalige Gruppen