ArticleThe journals of gerontology. Series A, Biological sciences and medical sciences2019
Impact of Aging and HIV Infection on the Function of the C-Type Lectin Receptor MINCLE in Monocytes.
Article in The journals of gerontology. Series A, Biological sciences and medical sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- HIV infection and immunosenescence: challenges and intervention strategies.BMC medicine · 2025Review
- Article
- Dectin-1 stimulation promotes a distinct inflammatory signature in the setting of HIV-infection and aging.Aging · 2023Article
- A comparison of curated gene sets versus transcriptomics-derived gene signatures for detecting pathway activation in immune cells.BMC bioinformatics · 2020Article
- Myeloid C-Type Lectin Receptors in Tuberculosis and HIV Immunity: Insights Into Co-infection?Frontiers in cellular and infection microbiology · 2020Review
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Both aging and HIV infection are associated with an enhanced pro-inflammatory environment that contributes to impaired immune responses and is mediated in part by innate immune pattern-recognition receptors. MINCLE is a C-type lectin receptor that recognizes trehalose-6,6'-dimycolate or "cord factor," the most abundant glycolipid in Mycobacterium tuberculosis. Here, we evaluated MINCLE function in monocytes in a cohort of HIV-infected and uninfected young (21-35 years) and older adults (≥60 years) via stimulation of peripheral blood mononuclear cells with trehalose-6,6-dibehenate, a synthetic analog of trehalose-6,6'-dimycolate and measurement of cytokine production (interleukin [IL]-10, IL-12, IL-6, tumor necrosis factor-α) by multicolor flow cytometry. Our studies show an age- and HIV-associated increase in cytokine multifunctionality of monocytes both at the population and single cell level that was dominated by IL-12, IL-10, and IL-6. These findings provide insight into the host response to M. tuberculosis and possible sources for the pro-inflammatory environment seen in aging and HIV infection.
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Registered trials
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