Co-ordinated expression of innate immune molecules during mouse neurulation

Mol Immunol. 2015 Dec;68(2 Pt A):253-60. doi: 10.1016/j.molimm.2015.09.004. Epub 2015 Sep 14.

Abstract

The innate immune system is the first line of defence against pathogens and infection. Recently, it has become apparent that many innate immune factors have roles outside of immunity and there is growing evidence that these factors play important functional roles during the development of a range of model organisms. Several studies have documented developmental expression of individual factors of the toll-like receptor and complement systems, and we recently demonstrated a key role for complement C5a receptor (C5aR1) signalling in neural tube closure in mice. Despite these emerging studies, a comprehensive expression analysis of these molecules in embryonic development is lacking. In the current study, we therefore, examined the expression of key innate immune factors in the early development period of neurulation (7.5-10.5dpc) in mice. We found that complement factor genes were differentially expressed during this period of murine development. Interestingly, the expression patterns we identified preclude activation of the classical and alternative pathways and formation of the membrane attack complex. Additionally, several other classes of innate immune molecules were expressed during the period of neurulation, including toll-like receptors (TLR-2, -3, -4 and -9), receptor for advanced glycation end-products (RAGE), and their signalling adapters (TRAF-4, TRAF-6, TAK-1 and MyD88). Taken together, this study highlights a number of innate immune factors as potential novel players in early embryonic development.

Keywords: Complement; Immunology; Neurulation; Toll-like receptors.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Complement Pathway, Alternative / genetics*
  • Complement Pathway, Classical / genetics*
  • Complement Pathway, Mannose-Binding Lectin / genetics*
  • Complement System Proteins / genetics*
  • Complement System Proteins / immunology
  • Embryo, Mammalian
  • Gene Expression Regulation, Developmental
  • Immunity, Innate*
  • In Situ Hybridization
  • MAP Kinase Kinase Kinases / genetics
  • MAP Kinase Kinase Kinases / immunology
  • Mice
  • Mice, Inbred C57BL
  • Myeloid Differentiation Factor 88 / genetics
  • Myeloid Differentiation Factor 88 / immunology
  • Neurulation / genetics
  • Neurulation / immunology*
  • Protein Isoforms / genetics
  • Protein Isoforms / immunology
  • Receptor for Advanced Glycation End Products / genetics
  • Receptor for Advanced Glycation End Products / immunology
  • Signal Transduction
  • TNF Receptor-Associated Factor 4 / genetics
  • TNF Receptor-Associated Factor 4 / immunology
  • Toll-Like Receptors / genetics
  • Toll-Like Receptors / immunology

Substances

  • Ager protein, mouse
  • Myd88 protein, mouse
  • Myeloid Differentiation Factor 88
  • Protein Isoforms
  • Receptor for Advanced Glycation End Products
  • TNF Receptor-Associated Factor 4
  • Toll-Like Receptors
  • Complement System Proteins
  • MAP Kinase Kinase Kinases
  • MAP kinase kinase kinase 7