IL-17A reprograms intestinal epithelial cells to facilitate HIV-1 replication and outgrowth in CD4+ T cells

Tomas Raul Wiche Salinas, Annie Gosselin, Laurence Raymond Marchand, Etiene Moreira Gabriel, Olivier Tastet, Jean Philippe Goulet, Yuwei Zhang, Dragos Vlad, Hanane Touil, Jean Pierre Routy, Mariana G. Bego, Mohamed El-Far, Nicolas Chomont, Alan L. Landay, Éric A. Cohen, Cécile Tremblay, Petronela Ancuta

Research output: Contribution to journalArticlepeer-review

3 Scopus citations


The crosstalk between intestinal epithelial cells (IECs) and Th17-polarized CD4+ T cells is critical for mucosal homeostasis, with HIV-1 causing significant alterations in people living with HIV (PLWH) despite antiretroviral therapy (ART). In a model of IEC and T cell co-cultures, we investigated the effects of IL-17A, the Th17 hallmark cytokine, on IEC ability to promote de novo HIV infection and viral reservoir reactivation. Our results demonstrate that IL-17A acts in synergy with TNF to boost IEC production of CCL20, a Th17-attractant chemokine, and promote HIV trans-infection of CD4+ T cells and viral outgrowth from reservoir cells of ART-treated PLWH. Importantly, the Illumina RNA-sequencing revealed an IL-17A-mediated pro-inflammatory and pro-viral molecular signature, including a decreased expression of type I interferon (IFN-I)-induced HIV restriction factors. These findings point to the deleterious features of IL-17A and raise awareness for caution when designing therapies aimed at restoring the paucity of mucosal Th17 cells in ART-treated PLWH.

Original languageEnglish (US)
Article number103225
Issue number11
StatePublished - Nov 19 2021
Externally publishedYes


  • Immune response
  • Immunology
  • Virology

ASJC Scopus subject areas

  • General


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