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It has been established that several mechanisms may contribute to the dysfunction of HBV-specific T cells, such as continuously high viral load and high antigen levels, suppressive cytokines including interleukin-10 (IL-10) and transforming growth factor- (TGF- ), dendritic cells (DCs) and regulatory T (Treg) cells, which were able to result in a progressive loss of T-cell function and cause HBV-specific T cells to become exhausted 7, 8 (Figure 1)

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NTR1 activation enhances neuronal excitability and improves spatial learning ability and memory in APP/PS1 transgenic mice [66]