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. 2014 Jan 13;111(7):2722–2727. doi: 10.1073/pnas.1317454111

Fig. 4.

Fig. 4.

Coligation of LILRB1 is essential for ADE. (A) Binding of LILRB1 to whole DENV or DENV E protein ectodomain. (B) Plaque titers following DENV-2 or ADE infection in the presence of soluble LILRB1 ectodomain (2 µM, 20 µM, 200 µM), 200 µM BSA, or no protein control. (C) Plaque titers following DENV-2 or ADE infection after LILRB1 or FcγRIIB knockdown. Numbers below Western blot indicate levels of proteins relative to LAMP-1. (D) Plaque titers following DENV-2 or ADE infection in THP-1.2R transfected with empty vector or vector expressing LILRB1, mutant LILRB1 (LILRB1MUT), or LILRB4. Numbers below Western blot indicate levels of proteins relative to LAMP-1. (E) Plaque titers following DENV-2–only and ADE infection of primary monocytes treated with sodium stibogluconate (SSG) or PBS control (dashed lines, shaded areas reflect SD). (F) Plaque titers following DENV-1–, -3, or -4–only and ADE infection of primary monocytes treated with SSG (0.138 mM) or PBS control. (G) Plaque titers in primary monocytes derived from PBMCs harvested from 12 healthy individuals and infected in vitro with either DENV-1 (n = 3), DENV-2 (n = 3), DENV-3 (n = 3), or DENV-4 (n = 3) opsonized with h4G2 antibodies at 72 hpi. PBMCs were either pretreated with polyclonal anti-LILRB1 antibody or isotype antibody control. Data are expressed as mean ± SD from three independent experiments. **P < 0.01, *P < 0.05.