The effects of immune protein CD3ζ development and degeneration of retinal neurons after optic nerve injury

PLoS One. 2017 Apr 25;12(4):e0175522. doi: 10.1371/journal.pone.0175522. eCollection 2017.

Abstract

Major histocompatibility complex (MHC) class I molecules and their receptors play fundamental roles in neuronal death during diseases. T-cell receptors (TCR) function as MHCI receptor on T-cells and both MHCI and a key component of TCR, CD3ζ, are expressed by mouse retinal ganglion cells (RGCs) and displaced amacrine cells. Mutation of these molecules compromises the development of RGCs. We investigated whether CD3ζ regulates the development and degeneration of amacrine cells after RGC death. Surprisingly, mutation of CD3ζ not only impairs the proper development of amacrine cells expressing CD3ζ but also those not expressing CD3ζ. In contrast to effects of MHCI and its receptor, PirB, on other neurons, mutation of CD3ζ has no effect on RGC death and starburst amacrine cells degeneration after optic nerve crush. Thus, unlike MHCI and PirB, CD3ζ regulates the development of RGCs and amacrine cells but not their degeneration after optic nerve crush.

MeSH terms

  • Amacrine Cells / immunology
  • Amacrine Cells / pathology
  • Animals
  • CD3 Complex / genetics
  • CD3 Complex / immunology*
  • Cell Death
  • Dendrites / immunology
  • Dendrites / pathology
  • Mice, Inbred C57BL
  • Mutation
  • Nerve Crush
  • Optic Nerve / cytology
  • Optic Nerve / immunology
  • Optic Nerve / pathology*
  • Optic Nerve Injuries / genetics
  • Optic Nerve Injuries / immunology
  • Optic Nerve Injuries / pathology*
  • Retinal Ganglion Cells / cytology
  • Retinal Ganglion Cells / immunology
  • Retinal Ganglion Cells / pathology*

Substances

  • CD3 Complex
  • CD3 antigen, zeta chain