New Paper: Macrophage Galactose Lectin is Critical for Kupffer Cells to Clear Aged Platelets

Congratulations to Platform 1 Co-Lead Dr. Paul Kubes on this recent publication!

Under naive conditions, platelets interact with and bind to Kupffer cells. SD-IVM of the mouse liver of CD41-YFPki/+ mice. Kupffer cells (blue) were stained using an anti-F4/80 antibody. Endogenous platelets (bright green) are labeled with YFP. Hepatocytes are shown in dark green (autofluorescence). Frame rate is 20 fps.

Abstract

Early life exposure to microbes plays an important role in immune system development. Germ-free mice, or mice colonized with a low-diversity microbiota, exhibit high serum IgE levels. An increase in microbial richness, providing it occurs in a critical developmental window early in life, leads to inhibition of this hygiene-induced IgE. However, whether this inhibition is dependent solely on certain microbial species, or is an additive effect of microbial richness, remains to be determined. Here we report that mice colonized with a combination of bacterial species with specific characteristics is required to inhibit IgE levels. These defined characteristics include the presence in early life, acetate production and immunogenicity reflected by induction of IgA. Suppression of IgE did not correlate with production of the short chain fatty acids propionate and butyrate, or induction of peripherally induced Tregs in mucosal tissues. Thus, inhibition of IgE induction can be mediated by specific microbes and their associated metabolic pathways and immunogenic properties.

Publication: Macrophage galactose lectin is critical for Kupffer cells to clear aged platelets. Deppermann C, Kratofil RM, Peiseler M, David BA, Zindel J, Silva Castanheira FVE, van der Wal F, Carestia A, Jenne CN, Marth JD, Kubes P. Journal of Experimental Medicine. 24 January 2020.