Figure 8.

Proposed scheme for BID-mediated apoptosis in astrocytes in NMO. Following culture of astrocytes with sera of NMO patients, we found an increase in the expression of BID, tp53, BAX, NOD-1, and TLR4. Increased BID levels may be linked to NMO pathogenesis through several pathways: The increase in BID can mediate the inflammation process in NMO by increasing NOD-1 and TLR4. The interaction of AQP4-IgG and AQP4 receptors on astrocytes leads to complement activation, necrosis/apoptosis, and DNA damage, which in turn may activate cell-cycle regulator tp53, leading to BID-mediated apoptosis. Other inflammatory factors in the sera of NMO patients can directly activate the BID pathway or indirectly by increasing DNA damage.