Commentary 10.1172/JCI121744

Vaginal epidermal dendritic cells: defense against HIV-1 or a safe haven?

Stephan Caucheteux1 and Vincent Piguet1,2

1Division of Dermatology, Department of Medicine, University of Toronto, Toronto, Ontario, Canada.

2Division of Dermatology, Women’s College Hospital, Toronto, Ontario, Canada.

Address correspondence to: Vincent Piguet, Dermatology, Department of Medicine, University of Toronto, Women’s College Hospital, 76 Grenville Street, Office 6425, Toronto, Ontario M5S 1B2, Canada. Phone: 416.323.6400 ext 5825; Email: vincent.piguet@utoronto.ca.

Find articles by Caucheteux, S. in: JCI | PubMed | Google Scholar

1Division of Dermatology, Department of Medicine, University of Toronto, Toronto, Ontario, Canada.

2Division of Dermatology, Women’s College Hospital, Toronto, Ontario, Canada.

Address correspondence to: Vincent Piguet, Dermatology, Department of Medicine, University of Toronto, Women’s College Hospital, 76 Grenville Street, Office 6425, Toronto, Ontario M5S 1B2, Canada. Phone: 416.323.6400 ext 5825; Email: vincent.piguet@utoronto.ca.

Find articles by Piguet, V. in: JCI | PubMed | Google Scholar

First published July 9, 2018 - More info

J Clin Invest. https://doi.org/10.1172/JCI121744.
Copyright © 2018, American Society for Clinical Investigation

First published July 9, 2018

Langerhans cells (LCs) are likely among the first targets of HIV-1 infection due to their localization in mucosal tissues. In their recent work, Pena-Cruz and colleagues were able to study HIV-1 infection in vaginal epithelial DCs (VEDCs), termed CD1a+ VEDCs. They show that VEDCs are distinct from other blood- and tissue-derived DCs or LCs because they express the protein langerin but not the lectin receptor DC-SIGN, and they do not have Birbeck granules. The results from this study indicate that HIV-1 using CXCR4 replicates poorly in VEDCs but that a higher replication for HIV-1 using CCR5 strains is supported by VDECs. Furthermore, Pena-Cruz and colleagues demonstrate that VDECs can represent a viral reservoir in HIV-1–infected virologically suppressed women. As such, VDECs may represent another sanctuary of viral persistence and can be an additional obstacle to viral eradication.

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