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Tuberculosis-associated IFN-I induces Siglec-1 on tunneling nanotubes and favors HIV-1 spread in macrophages

Abstract : While tuberculosis (TB) is a risk factor in HIV-1-infected individuals, the mechanisms by which Mycobacterium tuberculosis (Mtb) worsens HIV-1 pathogenesis remain scarce. We showed that HIV-1 infection is exacerbated in macrophages exposed to TB-associated microenvironments due to tunneling nanotube (TNT) formation. To identify molecular factors associated with TNT function, we performed a transcriptomic analysis in these macrophages, and revealed the upregulation of Siglec-1 receptor. Siglec-1 expression depends on Mtb-induced production of type I interferon (IFN-I). In co-infected non-human primates, Siglec-1 is highly expressed by alveolar macrophages, whose abundance correlates with pathology and activation of IFN-I/STAT1 pathway. Siglec-1 localizes mainly on microtubule-containing TNT that are long and carry HIV-1 cargo. Siglec
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https://hal-amu.archives-ouvertes.fr/hal-02995702
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Submitted on : Friday, November 20, 2020 - 6:23:19 PM
Last modification on : Monday, November 23, 2020 - 8:26:40 AM

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Maeva Dupont, Shanti Souriant, Luciana Balboa, Thien-Phong Vu Manh, Karine Pingris, et al.. Tuberculosis-associated IFN-I induces Siglec-1 on tunneling nanotubes and favors HIV-1 spread in macrophages. eLife, eLife Sciences Publication, 2020, 9, ⟨10.7554/eLife.52535⟩. ⟨hal-02995702⟩

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