**7. Conclusions**

58 Apoptosis and Medicine

**Figure 4.** Herp protein is expressed in BZLF1 positive EBV infected B cells.

**Figure 5.** Hypothetical mechanism of anti-dsDNA Ab induction.

infection may be a trigger of SLE.

lymphoid tissues. In addition, EBV-encoded latent membrane protein 2A (LMP2A) induces hypersensitivity to TLR stimulation, leading to activation of autoreactive B cells through the BCR/TLR pathway [90]. Immunization with the membrane fraction of EBV-transformed B cells elicited anti-dsDNA Abs as well as anti-Herp Abs and causes glomerular IgG deposition in BALB/c mice [62]. These observations support the hypothesis that EBV As dead cells are not only a source of intracellular antigens but also a source of proinflammatory molecules, it is likely that they play an important role in the generation of nephritogenic anti-dsDNA Abs. Herp was identified as a molecule directly involved in cell stress/death as the cause of anti-dsDNA Ab production. Further investigations are therefore needed to clarify the relationship between cell stress/death and the etiology of SLE.
