ifn-γ-dependent secretion of IL-10 from Th1 cells and microglia/macrophages contributes to functional recovery after spinal cord injury

Cell Death Dis. 2013 Jul 4;4(7):e710. doi: 10.1038/cddis.2013.234.

Abstract

Transfer of type-1 helper T-conditioned (Th1-conditioned) cells promotes functional recovery with enhanced axonal remodeling after spinal cord injury (SCI). This study explored the molecular mechanisms underlying the beneficial effects of pro-inflammatory Th1-conditioned cells after SCI. The effect of Th1-conditioned cells from interferon-γ (ifn-γ) knockout mice (ifn-γ(-/-) Th1 cells) on the recovery after SCI was reduced. Transfer of Th1-conditioned cells led to the activation of microglia (MG) and macrophages (MΦs), with interleukin 10 (IL-10) upregulation. This upregulation of IL-10 was reduced when ifn-γ(-/-) Th1 cells were transferred. Intrathecal neutralization of IL-10 in the spinal cord attenuated the effects of Th1-conditioned cells. Further, IL-10 is robustly secreted from Th1-conditioned cells in an ifn-γ-dependent manner. Th1-conditioned cells from interleukin 10 knockout (il-10(-/-)) mice had no effects on recovery from SCI. These findings demonstrate that ifn-γ-dependent secretion of IL-10 from Th1 cells, as well as native MG/MΦs, is required for the promotion of motor recovery after SCI.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adoptive Transfer
  • Animals
  • Cells, Cultured
  • Female
  • Glial Cell Line-Derived Neurotrophic Factor / metabolism
  • Immunotherapy, Adoptive
  • Interferon-gamma / physiology*
  • Interleukin-10 / metabolism*
  • Macrophages / metabolism*
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Microglia / metabolism*
  • Nerve Growth Factors / metabolism
  • Recovery of Function
  • Spinal Cord Injuries / immunology
  • Spinal Cord Injuries / therapy*
  • Th1 Cells / metabolism*
  • Th1 Cells / transplantation
  • Up-Regulation

Substances

  • Glial Cell Line-Derived Neurotrophic Factor
  • IL10 protein, mouse
  • Nerve Growth Factors
  • neurotropin 3, mouse
  • Interleukin-10
  • Interferon-gamma