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How immune cells in the brain coordinate their work
Infections in the brain can have serious consequences and are often fatal. The immune defence system works differently here than in the rest of the body. A team of researchers at TWINCORE – Centre for Experimental and Clinical Infection Research in Hanover – has now discovered, in collaboration with partners, which signalling pathways play a central role in communication between immune cells in the brain in their defence against viruses. The results have now been published in the Journal of Neuroinflammation.
Cells infected with viruses are recognised and eliminated by the body's own immune system. This prevents the virus from spreading and brings the infection under control. This process involves the interaction of various cells of the immune system. So-called myeloid cells, such as macrophages, recognise viruses and show T cells which cells are infected and need to be fought. In the brain, this role is performed by microglia.
‘Microglia cells are, so to speak, the project managers of the immune system in the brain, which coordinate the T cells,’ says Dr Andreas Pavlou, a scientist at the Institute for Experimental Infection Research at TWINCORE and first author of the study. ‘We have now been able to show that a specific signalling pathway in the cells is essential for this task.’ The transmission of biochemical signals in cells can trigger various metabolic reactions, such as the production of messenger substances or the provision of certain molecules on the cell surface. These receptors are recognized by other cells.
To test which cells in the brain play the decisive role, the researchers deleted the MAVS protein in different cell types in a mouse model. MAVS stands for ‘mitochondrial anti-viral signalling protein’. It is part of the RIG-I signalling pathway, which is important for the recognition of viruses. ‘When we deleted MAVS in other brain cells, such as neurons or astrocytes, we did not find any significant changes upon infection of the mice with the vesicular stomatitis virus.’ The immune defence continued to function. However, when MAVS was deactivated in the microglia cells, the infection spread very quickly in the brain.
‘The number of myeloid cells and infiltrating T cells in the brain was not reduced,’ says Pavlou. ‘However, the microglia had fewer signal receptors on their cell surface and the T cells showed abnormal metabolic activity.’ The researchers conclude that communication between the microglia and T cells is disrupted. ‘We were able to show that MAVS is an essential component in the communication between microglia cells and effector cells,’ says Pavlou. ‘Without this signal molecule, the microglia cells cannot fulfil their role as project managers of the immune response in the brain.’
‘These findings could help make therapeutic interventions for brain infections more effective in the future,’ says Prof. Ulrich Kalinke, Director of the Institute of Experimental Infection Research and Managing Director of TWINCORE. ‘We hope that this will lay the foundation for improved treatment of patients.’
Dr. Andreas Pavlou, andreas.pavlou@twincore.de
Prof. Dr. Ulrich Kalinke, ulrich.kalinke@twincore.de
Pavlou, A., Ghita, L., Mulenge, F. et al. MAVS signaling of long-lived brain-resident myeloid cells is needed during viral encephalitis to adjust the transcriptome of CNS infiltrating CD8+ T cells. J Neuroinflammation 22, 175 (2025).
https://doi.org/10.1186/s12974-025-03497-1
https://twincore.de/news/project-manager-of-the-immune-defence-in-the-brain | This press release on twincore.de
Dr. Andreas Pavlou, first author of the study, in the lab
Source: © TWINCORE/T. Damm
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