Transient expression of ZBTB32 in anti-viral CD8+T cells limits the magnitude of the effector response and the generation of memory

Virus infections induce cd8+t cell responses comprised of a large population of terminal effector cells and a smaller subset of long-lived memory cells. the transcription factors regulating the relative expansion versus the long-term survival potential of anti-viral cd8+t cells are not completely understood. we identified zbtb32 as a transcription factor that is transiently expressed in effector cd8+t cells. after acute virus infection,cd8+t cells deficient in zbtb32 showed enhanced virus-specific cd8+t cell responses,and generated increased numbers of virus-specific memory cells; in contrast,persistent expression of zbtb32 suppressed memory cell formation. the dysregulation of cd8+t cell responses in the absence of zbtb32 was catastrophic,as zbtb32-/-mice succumbed to a systemic viral infection and showed evidence of severe lung pathology. we found that zbtb32 and blimp-1 were co-expressed following cd8+t cell activation,bound to each other,and cooperatively regulated blimp-1 target genes eomes and cd27. these findings demonstrate that zbtb32 is a key transcription factor in cd8+effector t cells that is required for the balanced regulation of effector versus memory responses to infection. © 2017 shin et al.