IL-32 Drives the Differentiation of Cardiotropic CD4+ T Cells Carrying HIV DNA in People With HIV

Hardik Ramani, Annie Gosselin, Rémi Bunet, Mohammad Ali Jenabian, Mohamed Sylla, Amélie Pagliuzza, Carl Chartrand-Lefebvre, Jean Pierre Routy, Jean Philippe Goulet, Réjean Thomas, Benoit Trottier, Valérie Martel-Laferrière, Claude Fortin, Nicolas Chomont, Rémi Fromentin, Alan L. Landay, Madeleine Durand, Petronela Ancuta, Mohamed El-Far, Cecile Tremblay

Research output: Contribution to journalArticlepeer-review


Interleukin 32 (IL-32) is a potent multi-isoform proinflammatory cytokine, which is upregulated in people with HIV (PWH) and is associated with cardiovascular disease (CVD) risk. However, the impact of IL-32 isoforms on CD4 T-cell cardiotropism, a mechanism potentially contributing to heart inflammation, remains unknown. Here we show that IL-32 isoforms β and γinduce the generation of CCR4+CXCR3+ double positive (DP) memory CD4 T-cell subpopulation expressing the tyrosine kinase receptor c-Met, a phenotype associated with heart-homing of T cells. Our ex vivo studies on PWH show that the frequency of DP CD4 T cells is significantly higher in individuals with, compared to individuals without, subclinical atherosclerosis and that DP cells from antiretroviral-naive and treated individuals are highly enriched with HIV DNA. Together, these data demonstrate that IL-32 isoforms have the potential to induce heart-homing of HIV-infected CD4 T cells, which may further aggravate heart inflammation and CVD in PWH.

Original languageEnglish (US)
Pages (from-to)1277-1289
Number of pages13
JournalJournal of Infectious Diseases
Issue number5
StatePublished - May 15 2024
Externally publishedYes


  • cardiovascular disease
  • CD4 T cells
  • heart-homing
  • HIV
  • IL-32
  • inflammation

ASJC Scopus subject areas

  • General Medicine


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