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Styk1 expression is a hallmark of murine NK cells and other NK1.1+ subsets but is dispensable for NK-cell development and effector functions.

Sébastien Fauteux-DanielFabrice FaureMarie MarotelClair GearyCécile DaussyJoseph C SunThierry Walzer
Published in: European journal of immunology (2019)
To gain insight into the biology of NK cells, others and we previously identified the NK-cell signature, defined as the set of transcripts which expression is highly enriched in these cells compared to other immune subtypes. The transcript encoding the Serine/threonine/tyrosine kinase 1 (Styk1) is part of this signature. However, the role of Styk1 in the immune system is unknown. Here, we report the generation of a novel transgenic mouse model, in which Styk1 expression is invalidated and replaced by an EGFP reporter cassette. We demonstrated that Styk1 expression is a hallmark of NK cells and other NK1.1 expressing cells such as liver type 1 innate lymphoid cells (ILC1) and NK1.1+ γδ T cells. Styk1 expression is maintained by IL-15 in NK cells and negatively correlates with the expression of educating NK-cell receptors. Analysis of phosphorylation levels of mTOR substrates suggested that Styk1 could moderately contribute to the activity of the PI3K/Akt/mTOR pathway. However, Styk1-deficient NK cells develop normally and have normal in vitro and in vivo effector functions. Thus Styk1 expression is a hallmark of NK cells, ILC1 and NK1.1+ T cells but is dispensable for their development and immune functions.
Keyphrases
  • nk cells
  • poor prognosis
  • induced apoptosis
  • tyrosine kinase
  • binding protein
  • mouse model
  • cell cycle arrest
  • long non coding rna
  • oxidative stress
  • cell death
  • regulatory t cells
  • single cell