Toll-like receptor 7 (TLR7) is a ssRNA receptor that activates dendritic cells and macrophages upon ssRNA binding; however, little is known of its role in CD4+ T cells. We show here that hepatitis C virus (HCV) induces a dose dependent inhibition of cytokine production and expression of activation markers in CD4 T cells, which were restored by a TLR7-specific antagonist. These findings indicate that HCV induces CD4 T cell impairment via TLR7 which may contribute to failure of virus eradication, casting doubts on the use of TLR7 agonists to boost innate immunity in chronic RNA virus infections.

Hepatitis C virus inhibits CD4 T cell function via binding to Toll-like receptor 7

Ludovisi, S;MONDELLI, MARIO UMBERTO;
2017-01-01

Abstract

Toll-like receptor 7 (TLR7) is a ssRNA receptor that activates dendritic cells and macrophages upon ssRNA binding; however, little is known of its role in CD4+ T cells. We show here that hepatitis C virus (HCV) induces a dose dependent inhibition of cytokine production and expression of activation markers in CD4 T cells, which were restored by a TLR7-specific antagonist. These findings indicate that HCV induces CD4 T cell impairment via TLR7 which may contribute to failure of virus eradication, casting doubts on the use of TLR7 agonists to boost innate immunity in chronic RNA virus infections.
2017
Immunology incorporates cellular and molecular studies in immunology, as well as clinical research in immunopathology, infectious disease, autoimmunity, and allergy. Host-pathogen interactions in infectious disease, as well as experimental therapeutic applications of immunomodulating agents are also considered. Resources dealing primarily with the biology of microbial, viral, or parasitic pathogens are excluded and are covered in the Microbiology category.
Esperti anonimi
Inglese
Internazionale
STAMPA
137
108
111
4
no
7
info:eu-repo/semantics/article
262
Mele, D; Mantovani, S; Oliviero, B; Grossi, G; Ludovisi, S; Mondelli, MARIO UMBERTO; Varchetta, S.
1 Contributo su Rivista::1.1 Articolo in rivista
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11571/1181654
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