A research team at TWINCORE – Center for Experimental and Clinical Infection Research, together with partners, has identified a central signaling chain that controls the communication between immune cells during the defense against viruses in the brain. Infections in the brain are often severe and fatal because the immune defense functions differently there than in the rest of the body. The results of the study were published in the Journal of Neuroinflammation.

The immune system recognizes virus-infected cells and eliminates them to stop them from spreading. This process is based on the cooperation of various immune cells. Myeloid cells such as macrophages detect viruses and alert T cells to infected cells. In the brain, microglial cells take over this task and coordinate the T cells.

The researchers have deactivated the MAVS protein in various cell types in a mouse model. MAVS is part of the RIG-I signaling pathway, which is crucial for virus recognition. When deactivated in neurons or astrocytes, the immune defense remained intact after infection with the vesicular stomatitis virus. In microglial cells, however, deactivation led to a rapid spread of the infection.

The number of myeloid cells and infiltrating T cells in the brain remained unchanged, but microglial cells had fewer signaling receptors on their surface and T cells showed altered metabolic activities. This results in a disruption of communication between microglial cells and T cells. MAVS proves to be an essential component of this communication, without which microglial cells cannot fulfill their coordinating role.

These findings could improve future therapies for brain infections and contribute to more effective treatments.

Original Paper:

MAVS signaling of long-lived brain-resident myeloid cells is needed during viral encephalitis to adjust the transcriptome of CNS infiltrating CD8+ T cells | Journal of Neuroinflammation | Full Text

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