Fig. 1

LILRB2 and TREM2 are expressed on human microglia and they share ligands oAβ and PS. a. Immunofluorescence staining of AD patient brain tissue for LILRB2, IBA1 (microglia marker), amyloid plaques (6E10), GFAP (astrocyte marker), and TREM2. Scale bar = 20 μm. b. Titration curves of oAβ binding to LILRB2 and TREM2 Fc fusion proteins by ELISA. Data are presented as mean ± SD (n = 3 independent experiments). c. Titration curves of PS binding to LILRB2 and TREM2 Fc fusion proteins by ELISA. Data are presented as mean ± SD (n = 3 independent experiments). d. Representative immunostaining images of oAβ and PS binding to LILRB2 and TREM2 expressed on 293 T cell surface. Scale bar represents 5 μm. e-h. oAβ or PS binding to LILRB2 or TREM2 as measured by BLI. In the association stage, protein A sensor-captured Fc fusion proteins (LILRB2-Fc: e and f, TREM2-Fc: g and h) were incubated with oAβ (1 μM, e and g) or PS liposomes (1 mM, f and h), and the amount of oAβ (e and g) or PS (f and h) bound onto the sensors was presented as wavelength shift in nanometers (nm). The red dotted vertical line marks the transit from association stage to dissociation stage, where the sensors were dipped into kinetics buffer without ligands allowing free dissociation