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Tissue-like environments shape functional interactions of HIV-1 with immature dendritic cells

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Abele,  Tobias
Cellular Biophysics, Max Planck Institute for Medical Research, Max Planck Society;

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Göpfrich,  Kerstin
Cellular Biophysics, Max Planck Institute for Medical Research, Max Planck Society;

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Citation

Gallucci, L., Abele, T., Fronza, R., Stolp, B., Laketa, V., Ahmed, S. S., et al. (2023). Tissue-like environments shape functional interactions of HIV-1 with immature dendritic cells. EMBO Reports, 24(6): e56818, pp. 1-22. doi:10.15252/embr.202356818.


Cite as: https://hdl.handle.net/21.11116/0000-000D-1BFB-B
Abstract
Immature dendritic cells (iDCs) migrate in microenvironments with distinct cell and extracellular matrix densities in vivo and contribute to HIV-1 dissemination and mounting of antiviral immune responses. Here, we find that, compared to standard 2D suspension cultures, 3D collagen as tissue-like environment alters iDC properties and their response to HIV-1 infection. iDCs adopt an elongated morphology with increased deformability in 3D collagen at unaltered activation, differentiation, cytokine secretion, or responsiveness to LPS. While 3D collagen reduces HIV-1 particle uptake by iDCs, fusion efficiency is increased to elevate productive infection rates due to elevated cell surface exposure of the HIV-1-binding receptor DC-SIGN. In contrast, 3D collagen reduces HIV transfer to CD4 T cells from iDCs. iDC adaptations to 3D collagen include increased pro-inflammatory cytokine production and reduced antiviral gene expression in response to HIV-1 infection. Adhesion to a 2D collagen matrix is sufficient to increase iDC deformability, DC-SIGN exposure, and permissivity to HIV-1 infection. Thus, mechano-physical cues of 2D and 3D tissue-like collagen environments regulate iDC function and shape divergent roles during HIV-1 infection.