A short domain within Bcl-3 is responsible for its lymphocyte survival activity.

The NFkappaB factor Bcl-3 influences the survival of T cells when they are activated to take part in immune responses. Because treatment of mice with adjuvant results in the increased expression of Bcl-3 in T cells, where it has survival-promoting effects, Bcl-3 may be an important, limiting factor that is supplied to T cells only when they are contributing to an appropriate immune response to infection, and not when spuriously activated by self-antigens. Although Bcl-3 is a member of the NFkappaB/Rel/IkappaB family of transcription factors, the means by which it promotes T cell survival is not obvious because Bcl-3 is unique in having an ankyrin repeat domain, like inhibitory IkappaB proteins, while also possessing domains capable of transcriptional activation, like Rel proteins.