Macrophage plasticity and activation states drive differential expression of murine macrophage galactose-type lectin (MGL) orthologs

Abstract Macrophage plasticity and functional activation are critical to the broad array of macrophage-mediated functions that help determine disease outcomes. galactose-type lectin (MGL), a type-2 C-type receptor (CLR) primarily expressed on myeloid cells, has been shown play an anti-inflammatory role in innate response some infectious agents. Our lab recently demonstrated MGL-1 contributes antimicrobial murine model experimental tuberculosis. We further observe MGL-2 expression by RAW 264.7 macrophages similarly activated whole mycobacteria, but differentially regulated signaling through toll-like receptors (TLR) as well cytokine glucocorticoid receptors. find synthetic agonists microbial ligands TLR2, TLR4, TLR7 positively regulate expression, suggesting responsiveness repertoire antigens compared MGL-1. Additionally, differs between multiple bacterial species, both pathogenic non-pathogenic. Pathway inhibition experiments show upregulation stimuli occurs MyD88-dependent Toll-like signaling. Although classically associated with alternatively macrophages, we is M1 M2 polarized while restricted M2. These results demonstrate strong relationship macrophage states differential MGL indicate non-redundant roles immunity models disease. Supported grants from NIH, NIAID (R61 AI138328, R33 AI138328)