Inflammatory response in human tick-borne encephalitis: analysis of postmortem brain tissue

Area of Science:

• Neuroimmunology
• Virology
• Pathology

Background:

• Tick-borne encephalitis (TBE) is a viral infection affecting the central nervous system.
• The precise mechanisms of tissue destruction in TBE remain unclear.
• Understanding immune system involvement is crucial for TBE pathogenesis.

Purpose of the Study:

• To investigate the role of immunological mechanisms in TBE-related tissue damage.
• To identify specific immune cells and pathways involved in neuronal injury.

Main Methods:

• Immunohistochemical analysis of human TBE brain autoptic tissue (n=26).
• Evaluation of immune cell infiltration and activation markers.
• Assessment of neuronal damage markers like caspase-3.

Main Results:

• Predominance of macrophages/microglia and cytotoxic T cells in the brain parenchyma.
• Granzyme B-expressing lymphocytes were found in close proximity to TBE virus-infected neurons.
• Upregulation of caspase-3 in neurons, indicating apoptosis, was observed.

Conclusions:

• Cellular and humoral immune responses significantly contribute to tissue destruction in TBE.
• Granzyme B-releasing cytotoxic T cells and macrophages/microglia are key players in TBE neuropathology.
• Immune-mediated damage is a primary driver of TBE pathogenesis.