Quantitative expression of C-type lectin receptors in humans and mice

Int J Mol Sci. 2012;13(8):10113-10131. doi: 10.3390/ijms130810113. Epub 2012 Aug 14.

Abstract

C-type lectin receptors and their adaptor molecules are involved in the recognition of glycosylated self-antigens and pathogens. However, little is known about the species- and organ-specific expression profiles of these molecules. We therefore determined the mRNA expression levels of Dectin-1, MR1, MR2, DC-SIGN, Syk, Card-9, Bcl-10, Malt-1, Src, Dec-205, Galectin-1, Tim-3, Trem-1, and DAP-12 in 11 solid organs of human and mice. Mouse organs revealed lower mRNA levels of most molecules compared to spleen. However, Dec-205 and Galectin-1 in thymus, Src in brain, MR2, Card-9, Bcl-10, Src, and Dec-205 in small intestine, MR2, Bcl-10, Src, Galectin-1 in kidney, and Src and Galectin-1 in muscle were at least 2-fold higher expressed compared to spleen. Human lung, liver and heart expressed higher mRNA levels of most genes compared to spleen. Dectin-1, MR1, Syk and Trem-1 mRNA were strongly up-regulated upon ischemia-reperfusion injury in murine kidney. Tim3, DAP-12, Card-9, DC-SIGN and MR2 were further up-regulated during renal fibrosis. Murine kidney showed higher DAP-12, Syk, Card-9 and Dectin-1 mRNA expression during the progression of lupus nephritis. Thus, the organ-, and species-specific expression of C-type lectin receptors is different between mice and humans which must be considered in the interpretation of related studies.

Keywords: dendritic cells; infection; inflammation; innate immunity; macrophages; pattern recognition receptors.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Autoimmune Diseases / genetics*
  • Autoimmune Diseases / metabolism
  • Fibrosis / genetics*
  • Fibrosis / metabolism
  • Humans
  • Kidney Diseases / genetics*
  • Kidney Diseases / metabolism
  • Lectins, C-Type / genetics*
  • Lectins, C-Type / metabolism
  • Mice
  • Mice, Inbred C57BL
  • Organ Specificity
  • RNA, Messenger / genetics
  • Real-Time Polymerase Chain Reaction
  • Reperfusion Injury / genetics*
  • Reperfusion Injury / metabolism
  • Reverse Transcriptase Polymerase Chain Reaction

Substances

  • Lectins, C-Type
  • RNA, Messenger