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Regulation of asymmetric division and CD8+ T lymphocyte fate specification by protein kinase C? and protein kinase C?/?.


ABSTRACT: 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, PKC? and PKC?/?, 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.

SUBMITTER: Metz PJ 

PROVIDER: S-EPMC4340726 | biostudies-literature | 2015 Mar

REPOSITORIES: biostudies-literature

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Regulation of asymmetric division and CD8+ T lymphocyte fate specification by protein kinase Cζ and protein kinase Cλ/ι.

Metz Patrick J PJ   Arsenio Janilyn J   Kakaradov Boyko B   Kim Stephanie H SH   Remedios Kelly A KA   Oakley Katherine K   Akimoto Kazunori K   Ohno Shigeo S   Yeo Gene W GW   Chang John T JT  

Journal of immunology (Baltimore, Md. : 1950) 20150123 5


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, PKC  ...[more]

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