TLR agonists enhance responsiveness of inflammatory innate immune cells in HLA-B*57-positive HIV patients.
J Mol Med (Berl)
; 99(1): 147-158, 2021 01.
Article
en En
| MEDLINE
| ID: mdl-33278000
ABSTRACT
HLA-B*57 affects the course of HIV infection. Under antiretroviral therapy, its effects cannot be explained by outstandingly efficient T cell responses alone but may also involve cells of innate immunity. Studying in vitro stimulation with Pam3CSK4, E. coli LPS-B5 and CpG-ODN-2216, we observed greater induction of IL-6/IL-1beta double-positive CD14+CD16++ monocytes as well as IFN-gamma-positive cytotoxic CD56highCD16neg NK cells in HLA-B*57- versus HLA-B*44-positive HIV patients, while TNF-alpha induction remained unchanged. Differences were not seen in the other monocyte and NK cell subsets or in HLA-matched healthy controls. Our findings show that, in virally suppressed HIV infection, HLA-B*57 is associated with enhanced responsiveness of inflammatory innate immune cells to TLR ligands, possibly contributing to increased vulnerability in sepsis. KEY MESSAGES ⢠HLA-B*57 is a host factor affecting clinical outcomes of HIV infection. ⢠HLA-B*57 modifies inflammatory subsets of NK cells and monocytes in HIV infection. ⢠In HLA-B*57-positive HIV patients TLR agonists induce enhanced IL-6/IL-1beta in monocytes. ⢠NK cells from HLA-B*57 HIV patients release more IFN-gamma upon TLR costimulation. ⢠HLA-B*57 is linked to enhanced inflammatory responsiveness to TLR ligands.
Palabras clave
Texto completo:
1
Banco de datos:
MEDLINE
Asunto principal:
Células Asesinas Naturales
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Monocitos
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Linfocitos T
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Antígenos HLA-B
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Infecciones por VIH
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Receptores Toll-Like
Límite:
Adult
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Aged
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Aged80
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Female
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Humans
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Male
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Middle aged
Idioma:
En
Año:
2021
Tipo del documento:
Article