ArticleBMC immunology2025
HTLV-1-infected cells drive the differentiation of monocytes into macrophages in vitro.
Article in BMC immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- HTLV-1-Derived Exosomes Drive Transcriptional Reprogramming of Monocytes Toward a Mixed M1/M2 Phenotype in HAM/TSP.Pathogens (Basel, Switzerland) · 2026Article
- Macrophages in oncoviral infections: from immune regulators to therapeutic targets.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Integrated in vitro and multi-cohort cross-omics analysis of HTLV-1-associated lung pathology reveals a RelA-dependent mechanism for monocyte recruitment and differentiation.Molecular medicine (Cambridge, Mass.) · 2026Article
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8 authors.
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Abstract
backgroundThe human T-cell lymphotropic virus type 1 (HTLV-1) is a retrovirus that causes HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). HAM/TSP is a chronic inflammatory neurodegenerative disease characterized by leukocyte infiltration in the spinal cord. T-lymphocytes are the most important targets of HTLV-1 infection, but monocytes are also infected. Monocytes from HTLV-1-infected individuals exhibit important functional differences compared to cells from uninfected donors. Here, we investigated the effects of cell-cell physical contact and/or secreted factors of HTLV-1-infected cells in monocyte activation and differentiation.
methodsThe THP-1 human monocytic cell line was co-cultured with a human cell line transformed by HTLV-1 (MT-2) for 6 days. To determine the effects of co-culturing HTLV-1-infected cells in THP-1 monocytes cells were characterized by flow cytometry, immunofluorescence microscopy, and real-time PCR. Computational analysis of published transcriptomic datasets was realized to compare molecular profiles of macrophages and mononuclear cells from HTLV-1 carriers.
resultsCo-culture of monocytes with HTLV-1-infected cells induced macrophage differentiation and upregulation of typical macrophages-associated molecules (HLA-DR, CD80, and CD86), increased cytokine (TNFα, IL-6, and IL-1β) levels and their coding genes expression. Consistently, published transcriptomic datasets showed changes in important genes associated with inflammation during HAM/TSP in patients. The presence of HTLV-1-infected cells in the culture also induced significant upregulation of Interferon Stimulated Genes (ISG), indicating viral infection. Monocyte activation and differentiation into pro-inflammatory macrophages occurred in a cell-to-cell contact-independent manner, suggesting the role of factors secreted by infected cells.
conclusionsTogether, our results indicated that HTLV-1-infected cells induced monocyte differentiation into macrophages inflammatory, predominantly.
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