CD3+ T-cell: CD14+ monocyte complexes are dynamic and increased with HIV and glucose intolerance

Persistent systemic inflammation is associated with an elevated risk of cardiometabolic diseases. However, the characteristics of the innate and adaptive immune systems in individuals who develop these conditions remain poorly defined. Doublets, or cell-cell complexes, are routinely eliminated from flow cytometric and other immune phenotyping analyses, which limits our understanding of their relationship to disease states. Using well-characterized clinical cohorts, including participants with controlled human immunodeficiency virus (HIV) as a model for chronic inflammation and increased immune cell interactions, we show that circulating CD14+ monocytes complexed to CD3+ T cells are dynamic, biologically relevant, and increased in individuals with diabetes after adjusting for confounding factors. The complexes form functional immune synapses with increased expression of proinflammatory cytokines and greater glucose utilization. Furthermore, in persons with HIV, the CD3+ T cell: CD14+ monocyte complexes had more HIV copies compared to matched CD14+ monocytes or CD4+ T cells alone. Our results demonstrate that circulating CD3+ T-cell: CD14+ monocyte pairs represent dynamic cellular interactions that may contribute to inflammation and cardiometabolic disease pathogenesis. CD3+ T-cell: CD14+ monocyte complexes may originate or be maintained, in part, by chronic viral infections. These findings provide a foundation for future studies investigating mechanisms linking T cell-monocyte cell-cell complexes to developing immune-mediated diseases, including HIV and diabetes.

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Publication Details

Journal
The Journal of Immunology
Published
2025-02-28
DOI
https://doi.org/10.1093/jimmun/vkae054
Citations
2
Primary Topic
Immune Cell Function and Interaction
Type
article
Field-Weighted Citation Impact
1.59
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article

CD3+ T-cell: CD14+ monocyte complexes are dynamic and increased with HIV and glucose intolerance

Jared Oakes, Antentor Hinton, Stephen Priest, Christian M. Warren et al.
2 citations
The Journal of Immunology
Immune Cell Function and Interaction
1.59
article

CD3+ T-cell: CD14+ monocyte complexes are dynamic and increased with HIV and glucose intolerance

Jared Oakes, Antentor Hinton, Stephen Priest, Christian M. Warren, Xiuqi Zhang, David G. Harrison, Samuel Bailin, Joey Stolze, Tarek Absi, Yan Ru Su, Leslie M. Meenderink, Tecla M. Temu, Suman Pakala, Cindy Nochowicz, Curtis L. Gabriel, Quanhu Sheng, Celestine N. Wanjalla, Abha Chopra, Spyros A. Kalams, Erin M. Wilfong, Simon Alexander Mallal, Sara Gianella, Kit Neikirk, Heather K. Beasley, Elizabeth Jane Phillips, Mona Mashayekhi, Jianqiang Shao, Rama Gangula, John R. Koethe, Annet Kirabo, Laventa M. Obare, Joshua D. Simmons
article en
2 citations

Abstract

Persistent systemic inflammation is associated with an elevated risk of cardiometabolic diseases. However, the characteristics of the innate and adaptive immune systems in individuals who develop these conditions remain poorly defined. Doublets, or cell-cell complexes, are routinely eliminated from flow cytometric and other immune phenotyping analyses, which limits our understanding of their relationship to disease states. Using well-characterized clinical cohorts, including participants with controlled human immunodeficiency virus (HIV) as a model for chronic inflammation and increased immune cell interactions, we show that circulating CD14+ monocytes complexed to CD3+ T cells are dynamic, biologically relevant, and increased in individuals with diabetes after adjusting for confounding factors. The complexes form functional immune synapses with increased expression of proinflammatory cytokines and greater glucose utilization. Furthermore, in persons with HIV, the CD3+ T cell: CD14+ monocyte complexes had more HIV copies compared to matched CD14+ monocytes or CD4+ T cells alone. Our results demonstrate that circulating CD3+ T-cell: CD14+ monocyte pairs represent dynamic cellular interactions that may contribute to inflammation and cardiometabolic disease pathogenesis. CD3+ T-cell: CD14+ monocyte complexes may originate or be maintained, in part, by chronic viral infections. These findings provide a foundation for future studies investigating mechanisms linking T cell-monocyte cell-cell complexes to developing immune-mediated diseases, including HIV and diabetes.

The Journal of ImmunologyVol. 214(3)
University of Iowa (US), Murdoch University (AU), Vanderbilt University (US), University of Washington (US), University of California San Diego (US), VA Tennessee Valley Healthcare System (US), Vanderbilt University Medical Center (US)
Openalex Percentile: Top 19%
Immune Cell Function and Interaction
1.59
DOIOpen Access PDFOpenAlex
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