KIR2DL2 inhibitory pathway enhances Th17 cytokine secretion by NK cells in response to herpesvirus infection in multiple sclerosis patients

J Neuroimmunol. 2016 May 15:294:1-5. doi: 10.1016/j.jneuroim.2016.03.007. Epub 2016 Mar 18.

Abstract

We have previously demonstrated that multiple sclerosis (MS) patients with KIR2DL2 expression on Natural killer (NK) cells are more susceptible to herpes simplex virus 1 (HSV-1) infection. We explored cytokine expression by NK cells during HSV-1 infection in association with KIR2DL2 expression. MS KIR2DL2(+) NK cells failed to control HSV-1 infection and secreted high levels of Th17 cytokines, while MS KIR2DL2(-) NK cells released Th1 cytokines, mainly IFN-gamma. Our data showed, for the first time, a peculiar Th17 cytokine secretion by MS KIR2DL2(+) NK cells in the presence of HSV-1 infection, that could be implicated in MS pathogenesis.

Keywords: Herpesvirus; Host/pathogens interactions; Inhibitory receptor; NK cells; Th17.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Cells, Cultured
  • Cytokines / metabolism*
  • Female
  • Herpes Simplex*
  • Humans
  • Killer Cells, Natural / metabolism*
  • Killer Cells, Natural / virology
  • Lymphocyte Activation
  • Male
  • Middle Aged
  • Multiple Sclerosis, Relapsing-Remitting / pathology*
  • Multiple Sclerosis, Relapsing-Remitting / virology
  • RNA, Messenger / metabolism
  • Receptors, KIR2DL2 / genetics
  • Receptors, KIR2DL2 / metabolism*
  • Th17 Cells / metabolism
  • Viral Load / methods

Substances

  • Cytokines
  • KIR2DL2 protein, human
  • RNA, Messenger
  • Receptors, KIR2DL2