[Go to this article.]

Figure 6
HDL preserves DC differentiation and function during mycobacterial infection. (A) Effect of HDL on oxPAPC-mediated inhibition of CD1b⁺ DC differentiation. Data are representative of 2 experiments. Numbers within plots denote percent CD1b⁺ cells. (B) Effect of HDL on mycobacteria-mediated inhibition of CD1b⁺ DC differentiation. Monocytes were infected with BCG alone or with 150 μg/ml HDL. Data are representative of more than 6 experiments. (C) Effect of HDL on CD1b-restricted mycobacterial antigen presentation by M. tuberculosis H37Ra–infected DCs. T cell activation was assessed by IFN-γ release. Data (mean ± SEM of triplicate wells) are representative of 3 experiments. *P < 0.001. (D) Effect of HDL from L-lep patients on CD1b⁺ DC differentiation. Left: Representative cell surface staining comparing normal and L-lep HDL (50 μg/ml) with and without M. tuberculosis H37Ra (M. tb) infection (MOI, 0.1). Numbers within plots denote percent CD1b⁺ cells. Right: Percent CD1b⁺ DCs relative to uninfected. Data represent mean ± SEM of 3 experiments using HDL from normal (n = 3) and L-lep (n = 5) donors. **P ≤ 0.02. (E) Functional assessment of HDL from leprosy patients. Monocyte chemotactic activity in normal (NL; n = 5) and leprosy HDL (L-lep and T-lep, n = 12 per group). ***P = 0.001. L-lep versus T-lep HDL was not significant (P = 0.23). (F) Reverse cholesterol transport with normal and leprosy HDL. Cholesterol efflux with normal (n = 8), L-lep (n = 11), and T-lep (n = 11) HDL (25 μg/ml). ***P = 0.001; ^#P = 0.049. (G) Effect of normal and leprosy HDL on CD1b⁺ DC differentiation. Normal (n = 7), L-lep (n = 8), and T-lep (n = 11) HDL (50 μg/ml) was added to differentiating monocytes, and CD1b⁺ DCs were quantified by flow cytometry. ***P = 0.001; ^##P = 0.02.