| First Author | Metz PJ | Year | 2015 |
| Journal | J Immunol | Volume | 194 |
| Issue | 5 | Pages | 2249-59 |
| PubMed ID | 25617472 | Mgi Jnum | J:232677 |
| Mgi Id | MGI:5779785 | Doi | 10.4049/jimmunol.1401652 |
| Citation | Metz PJ, et al. (2015) Regulation of asymmetric division and CD8+ T lymphocyte fate specification by protein kinase Czeta and protein kinase Clambda/iota. J Immunol 194(5):2249-59 |
| abstractText | During an immune response against a microbial pathogen, activated naive T lymphocytes give rise to effector cells that provide acute host defense and memory cells that provide long-lived immunity. It has been shown that T lymphocytes can undergo asymmetric division, enabling the daughter cells to inherit unequal amounts of fate-determining proteins and thereby acquire distinct fates from their inception. In this study, we show that the absence of the atypical protein kinase C (PKC) isoforms, PKCzeta and PKClambda/iota, disrupts asymmetric CD8(+) T lymphocyte division. These alterations were associated with aberrant acquisition of a pre-effector transcriptional program, detected by single-cell gene expression analyses, in lymphocytes that had undergone their first division in vivo and enhanced differentiation toward effector fates at the expense of memory fates. Together, these results demonstrate a role for atypical PKC in regulating asymmetric division and the specification of divergent CD8(+) T lymphocyte fates early during an immune response. |
