ArticleClinical immunology (Orlando, Fla.)2017
CD4+ T cells from HIV-1 patients with impaired Th1 effector responses to Mycobacterium tuberculosis exhibit diminished histone and nucleoprotein signatures.
Article in Clinical immunology (Orlando, Fla.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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.
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Who cites it
3 citing papers in PubMed, 4 citations in OpenAlex.
- T Cell Responses during Human Immunodeficiency Virus/Vaccines · 2024Review
- Dysregulation of the Immune System in HIV/HCV-Coinfected Patients According to Liver Stiffness Status.Cells · 2018Article
- Transcriptional regulation mediated by H2A.Z via ANP32e-dependent inhibition of protein phosphatase 2A.Biochimica et biophysica acta. Gene regulatory mechanisms · 2018Article
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Authors and funding
3 authors at 1 institution in 1 country.
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Abstract
HIV+ patients have an increased risk for tuberculosis disease despite clinical management with ARTs. We established a culture model of Mtb-infection in PBMCs from HIV+ PPD+ donors on suppressive ART (median 6.4years) with negligible viral loads (median<50copies/mL) and stable CD4+ T cell counts (517cells/mm^3). We observed that HIV+ patient lymphocytes harbored a recruitment defect to Mtb-infected monocytes. To investigate these immune defects on a per cell basis, purified CD4+ T cells from HIV patients were assessed by label-free quantification protein mass spectrometry. CD4+ T cells from HIV patients displayed diminished nucleoprotein levels - notably of histone variant H2a.Z and ribonucleoprotein A1. Only within healthy donors, transcriptional regulatory histone variant H2a.Z expression was correlated to the extent of IFN-γ induction upon Mtb-infection. Our findings may explain why HIV patients exhibit prolonged immune cell dysfunction despite suppressive ART, and implicate a per cell defect of CD4+ T cells.
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