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PD-L1 (B7-H1) regulation in zones of axonal degeneration

Michael Lipp1, Christine Brandt, Faramarz Dehghani

  • 1Institute of Cell Biology and Neurobiology, Department Exp. Neuroimmunology, Charité, 10098 Berlin, Germany.

Neuroscience Letters
|September 11, 2007
PubMed

Fibre tract injury evokes recruitment of antigen-presenting- and T cells, but does not cause autoimmune demyelination. This implies that immune tolerance to myelin is actively maintained or readily re-established. Using entorhinal cortex lesion (ECL) to induce axonal degeneration in the hippocampus of adult mice, we studied the induction of B7-H1 (PD-L1) in zones of axonal degeneration. This member of the B7-family has been shown to be expressed on parenchymal cells of various organs, where it strongly down-modulates the activity of T cells. Real-time reverse transcriptase (RT)-PCR revealed low mRNA levels in brain compared to lung and spleen under normal conditions. After ECL, a twofold increase could be observed. Immunocytochemistry revealed astrocytes as source of B7-H1, while immune positive microglia were not detected. Thus, axonal degeneration induces astrocytes to express B7-H1, a potent inhibitor of effector T cells.

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