The Toll-like receptors are the first line of the host response to pathogens, representing an essential com- ponent of the innate and adaptive immune response. They recognize different pathogens and trigger re- sponses directed at eliminating the invader and at de- veloping immunologic long-term memory, ultimately affecting viral pathogenesis. In viral infections, sensing of nucleic acids and/or viral structural proteins generally induces a protective immune response. Thus, it is not surprising that many viruses have developed strategies to evade or counteract signaling through the Toll-like receptor pathways, to survive the host defense machin- ery and ensure propagation. Thus, Toll-like receptor engagement can also be part of viral pathogenic mech- anisms. Evidence for a direct interaction of Toll-like receptors with human immunodeficiency virus type 1 (HIV-1) structures has started to be achieved, and alterations of their expression and function have been described in HIV-1–positive subjects. Furthermore, Toll- like receptor triggering by bacterial and viral ligands have been described to modulate HIV-1 replication and host response, leading to protective or detrimental effects. This review covers major advances in the field of HIV-1 interplay with Toll-like receptors, focusing on human myeloid cells (e.g., monocytes/macrophages and den- dritic cells). The role of this interaction in the dysregula- tion of myeloid cell function and in dictating aspects of the multifaceted pathogenesis of acquired immunodefi- ciency syndrome will be discussed

Interplay between hiv-1 and toll-like receptors in human myeloid cells: Friend or foe in hiv-1 pathogenesis? / Donninelli, Gloria; Gessani, Sandra; Cornò, Manuela Del. - In: JOURNAL OF LEUKOCYTE BIOLOGY. - ISSN 0741-5400. - STAMPA. - 99:1(2016), pp. 97-105. [10.1189/jlb.4VMR0415-160R]

Interplay between hiv-1 and toll-like receptors in human myeloid cells: Friend or foe in hiv-1 pathogenesis?

DONNINELLI, GLORIA;
2016

Abstract

The Toll-like receptors are the first line of the host response to pathogens, representing an essential com- ponent of the innate and adaptive immune response. They recognize different pathogens and trigger re- sponses directed at eliminating the invader and at de- veloping immunologic long-term memory, ultimately affecting viral pathogenesis. In viral infections, sensing of nucleic acids and/or viral structural proteins generally induces a protective immune response. Thus, it is not surprising that many viruses have developed strategies to evade or counteract signaling through the Toll-like receptor pathways, to survive the host defense machin- ery and ensure propagation. Thus, Toll-like receptor engagement can also be part of viral pathogenic mech- anisms. Evidence for a direct interaction of Toll-like receptors with human immunodeficiency virus type 1 (HIV-1) structures has started to be achieved, and alterations of their expression and function have been described in HIV-1–positive subjects. Furthermore, Toll- like receptor triggering by bacterial and viral ligands have been described to modulate HIV-1 replication and host response, leading to protective or detrimental effects. This review covers major advances in the field of HIV-1 interplay with Toll-like receptors, focusing on human myeloid cells (e.g., monocytes/macrophages and den- dritic cells). The role of this interaction in the dysregula- tion of myeloid cell function and in dictating aspects of the multifaceted pathogenesis of acquired immunodefi- ciency syndrome will be discussed
2016
Innate immunity; Pathogen recognition; Cell Biology; Immunology
01 Pubblicazione su rivista::01g Articolo di rassegna (Review)
Interplay between hiv-1 and toll-like receptors in human myeloid cells: Friend or foe in hiv-1 pathogenesis? / Donninelli, Gloria; Gessani, Sandra; Cornò, Manuela Del. - In: JOURNAL OF LEUKOCYTE BIOLOGY. - ISSN 0741-5400. - STAMPA. - 99:1(2016), pp. 97-105. [10.1189/jlb.4VMR0415-160R]
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/856400
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