Trial reportThe Journal of clinical investigation2018
Cycling CD4+ T cells in HIV-infected immune nonresponders have mitochondrial dysfunction.
Trial report in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
57 citing papers in PubMed, 1 synthesis or guideline pooled it, 91 citations in OpenAlex.
- Pooled it
- Elucidating the mechanism underlying incomplete immune recovery in people living with HIV through CD4⁺ and CD8⁺ T cell multi-omics.Molecular medicine (Cambridge, Mass.) · 2026Article
- Roles of mitophagy and immune infiltration in Parkinson's disease: new perspectives from bioinformatics analysis and A53T transgenic mice.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Article
- Immune cells harbor their own microbiome-derived metabolome: a new layer of immunometabolic regulation.Frontiers in immunology · 2026Review
- Age-Associated Expansion of HIV/SIV Reservoirs in People With HIV and SIV-Infected Macaques.Aging cell · 2025Article
- The Pathogenic Role of T Cell Metabolism and its Effect on Immune Senescence in Autoimmune Diseases and Infection.Clinical reviews in allergy & immunology · 2025Review
- Immune cell subset profiling and metabolic dysregulation define the divergent immune microenvironments in HIV immunological non-responders.Clinical and translational medicine · 2025Article
- Article
- Multi-omics dissection of metabolic dysregulation associated with immune recovery in people living with HIV-1.Journal of translational medicine · 2025Article
- How to properly define immunological nonresponse to antiretroviral therapy in people living with HIV? an integrative review.Frontiers in immunology · 2025Review
- T Cell Aging: An Important Target for Perioperative Immunomodulation.Clinical interventions in aging · 2025Review
- Naturally arising memory-phenotype CD4Science advances · 2024Article
- Regulatory T cells modulate monocyte functions in immunocompetent antiretroviral therapy naive HIV-1 infected people.BMC immunology · 2024Article
- Circulating GDF-15: a biomarker for metabolic dysregulation and aging in people living with HIV.Frontiers in aging · 2024Article
- Incomplete immune reconstitution and its predictors in people living with HIV in Wuhan, China.BMC public health · 2023Article
- ROS-Induced Mitochondrial Dysfunction in CD4 T Cells from ART-Controlled People Living with HIV.Viruses · 2023Article
- Profound phenotypic and epigenetic heterogeneity of the HIV-1-infected CD4Nature immunology · 2023Article
- Cellular and molecular insights into incomplete immune recovery in HIV/AIDS patients.Frontiers in immunology · 2023Review
- Identification of Potential Diagnostic Genes of HIV-Infected Immunological Non-Responders on Bioinformatics Analysis.Journal of inflammation research · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
20 authors at 7 institutions in 3 countries.
Funding
Abstract
Immune nonresponder (INR) HIV-1-infected subjects are characterized by their inability to reconstitute the CD4+ T cell pool after antiretroviral therapy. This is linked to poor clinical outcome. Mechanisms underlying immune reconstitution failure are poorly understood, although, counterintuitively, INRs often have increased frequencies of circulating CD4+ T cells in the cell cycle. While cycling CD4+ T cells from healthy controls and HIV+ patients with restored CD4+ T cell numbers complete cell division in vitro, cycling CD4+ T cells from INRs do not. Here, we show that cells with the phenotype and transcriptional profile of Tregs were enriched among cycling cells in health and in HIV infection. Yet there were diminished frequencies and numbers of Tregs among cycling CD4+ T cells in INRs, and cycling CD4+ T cells from INR subjects displayed transcriptional profiles associated with the impaired development and maintenance of functional Tregs. Flow cytometric assessment of TGF-β activity confirmed the dysfunction of Tregs in INR subjects. Transcriptional profiling and flow cytometry revealed diminished mitochondrial fitness in Tregs among INRs, and cycling Tregs from INRs had low expression of the mitochondrial biogenesis regulators peroxisome proliferator-activated receptor γ coactivator 1-α (PGC1α) and transcription factor A for mitochondria (TFAM). In vitro exposure to IL-15 allowed cells to complete division, restored the expression of PGC1α and TFAM, and regenerated mitochondrial fitness in the cycling Tregs of INRs. Our data suggest that rescuing mitochondrial function could correct the immune dysfunction characteristic of Tregs in HIV-1-infected subjects who fail to restore CD4+ T cells during antiretroviral therapy.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.