Modifying CREM expression in wild type or lupus-prone mice (e.g., B6.lpr and MRL.lpr mice) will provide a more global understanding of the involvement of CREMα and its isoforms in vivo. CREM-deficient mice have already unraveled the involvement of CREM during spermatogenesis [58]. CREM-deficient mice and transgenic approaches, such as overexpressing CREMα in T lymphocytes, will help to decipher whether CREMα plays a role during the priming and differentiation of immune cells in health and autoimmunity. Targeting CREMα with small interfering RNAs (siRNAs) in vivo will also help to assess its therapeutic potential in SLE.
