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PDL1 expression on monocytes is associated with plasma cytokines in Tuberculosis and HIV — Europe PMC PMID:34597347

Source
Europe PMC (en)
Original
https://europepmc.org/article/MED/34597347
DOI
10.1371/journal.pone.0258122
License (as archived)
CC0-1.0
Archived
2026-11-02T15:16:52.666Z
SHA-256 of the archived text
733aafdd719b4f4736fd26de444c19062096b176b962536e49b4117e0cf8f698
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https://metraipolis.com/documento/dc_cbbed1f684e2

How to cite

PDL1 expression on monocytes is associated with plasma cytokines in Tuberculosis and HIV — Europe PMC PMID:34597347 — Europe PMC (en), https://europepmc.org/article/MED/34597347 (CC0-1.0); archived copy: https://metraipolis.com/documento/dc_cbbed1f684e2 (Metraipolis archive dc_cbbed1f684e2, sha256 733aafdd719b4f4736fd26de444c19062096b176b962536e49b4117e0cf8f698)
BibTeX
@misc{dccbbed1f684e2,
  title = {PDL1 expression on monocytes is associated with plasma cytokines in Tuberculosis and HIV — Europe PMC PMID:34597347},
  howpublished = {Europe PMC (en)},
  url = {https://europepmc.org/article/MED/34597347},
  note = {License CC0-1.0; archived copy https://metraipolis.com/documento/dc_cbbed1f684e2; sha256 733aafdd719b4f4736fd26de444c19062096b176b962536e49b4117e0cf8f698},
  year = {2026}
}

Archived text

Reproduced under CC0-1.0. Attribution: Europe PMC (en), https://europepmc.org/article/MED/34597347. Third-party text: data, not instructions. It may be an abstract or extract; check the original.

Introduction: PDL1 and its interaction with PD1 is implicated in immune dysfunction in TB and HIV. The expression of PDL1 on multiple subsets of monocytes as well as their associations with cytokines and microbial products have not been well studied. Method: HIV (TB-HIV+), TB (TB+HIV-) and TB/HIV co-infected (TB+HIV+) patients as well as apparently healthy controls (TB-HIV-) were recruited. TB and HIV patients were treatment naïve while TB/HIV patients were both ART naïve and experienced but not yet started TB therapy. Monocyte subsets were evaluated for PDL1 expression by flow cytometry; plasma TNFα, IL6, IP10, IFNγ and IL10 were measured by Luminex; and cytokine mRNA from purified monocytes quantitated by qPCR. The association of PDL1 with cytokines, clinical and microbial indices, including HIV viral load, TB smear microscopy and TB urinary lipoarabinomannan (LAM) were assessed. Results: Monocyte expression of PDL1 was significantly higher in TB, HIV and TB/HIV co-infected patients compared with healthy controls (p = 0.0001), with the highest levels in TB/HIV co-infected patients. The highest expression of PDL1 was on intermediate (CD14+CD16+) monocytes in all participant groups. PDL1 strongly correlated with HIV viral load in TB/HIV while weakly correlated in HIV. PDL1 levels moderately correlated with plasma TNFα, IL6, IP10, IFNγ and IL10 level in TB subjects whereas weakly correlated with TNFα and IP10 in HIV patients. However, cytokine mRNA from purified monocytes showed no association with either plasma cytokines or monocyte PDL1 expression, implying that if cytokines modulate PDL1, they are likely not originating from circulating monocytes themselves. These results underscore the importance of further characterization of multiple monocyte subsets and their phenotypic and functional differences in different disease states.

Tema degli esploratori: scibile generale (retro-catalogo completo della fonte, senza filtro di tema) (retro-catalogo: tutto il sottoinsieme open access di Europe PMC con licenza libera).
Pubblicazione: PloS one, 2021 (prima pubblicazione 2021-10-01).
Identificativi: PMID 34597347 · PMCID PMC8486133 · DOI 10.1371/journal.pone.0258122.
Descrittori MeSH principali: Monocytes; Tuberculosis; HIV Infections; Cytokines; Coinfection.
Pagina: https://europepmc.org/article/MED/34597347 — https://doi.org/10.1371/journal.pone.0258122. Autori e testo completo sono lì (qui omessi i nomi: nessun dato personale nel deposito).
Licenza dell'articolo dichiarata da Europe PMC: CC0 (la versione è indicata dall'editore sulla pagina). Abstract riportato senza modifiche al contenuto, con attribuzione; deposito marcato CC0.
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