Affordable Access

Publisher Website

Interleukin-15 improves cytotoxicity of natural killer cells via up-regulating NKG2D and cytotoxic effector molecule expression as well as STAT1 and ERK1/2 phosphorylation

Authors
Publisher
Elsevier Ltd
Publication Date
Volume
42
Issue
1
Identifiers
DOI: 10.1016/j.cyto.2008.01.003
Keywords
  • Cytokine
  • Nk Cells
  • Nkrs
  • Cytotoxicity
  • Signal Transduction
Disciplines
  • Biology
  • Design
  • Medicine

Abstract

Abstract NK cells are crucial components of the innate immune system, providing a first line of defense against infectious pathogens and tumors. IL-15 is the major physiologic growth factor responsible for NK cell differentiation, survival and cytolytic activity of mature NK cells. However, the exact regulatory mechanism of IL-15 on NK cell function is still unclear. In this study, we try to investigate the mechanism of IL-15 on NK cytolysis. Our results demonstrate that IL-15 treatment increased NKG2D transcripts and surface expression in NK cells. NKG2D or MICA blockade attenuated the up-regulation of IL-15 on NK cytolysis, demonstrating that the up-regulatory effect of IL-15 on NK cytolysis is at least partly dependent of the interaction of NKG2D and MICA. Furtherfore, IL-15 augmented the expression of cytotoxic effector molecules (TRAIL and Perforin) and the phosphorylation of STAT1 and ERK1/2, which may also contribute the NK lysis. These results may have therapeutic implications when designing cytokine immunotherapy against cancer.

There are no comments yet on this publication. Be the first to share your thoughts.