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Triggering of TLR‐3, ‐4, NOD2, and DC‐SIGN reduces viral replication and increases T‐cell activation capacity of HIV‐infected human dendritic cells
Author(s) -
Cardinaud Sylvain,
Urrutia Alejandra,
Rouers Angeline,
Coulon PierreGrégoire,
Kervevan Jérome,
Richetta Clémence,
Bet Anne,
Maze Emmanuel A.,
Larsen Martin,
Iglesias MariaCandela,
Appay Victor,
GraffDubois Stéphanie,
Moris Arnaud
Publication year - 2017
Publication title -
european journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.272
H-Index - 201
eISSN - 1521-4141
pISSN - 0014-2980
DOI - 10.1002/eji.201646603
Subject(s) - dc sign , biology , dendritic cell , virology , nod2 , replication (statistics) , viral replication , sign (mathematics) , human immunodeficiency virus (hiv) , t cell , microbiology and biotechnology , immunology , virus , immune system , innate immune system , mathematical analysis , mathematics
A variety of signals influence the capacity of dendritic cells (DCs) to mount potent antiviral cytotoxic T‐cell (CTL) responses. In particular, innate immune sensing by pathogen recognition receptors, such as TLR and C‐type lectines, influences DC biology and affects their susceptibility to HIV infection. Yet, whether the combined effects of PPRs triggering and HIV infection influence HIV‐specific (HS) CTL responses remain enigmatic. Here, we dissect the impact of innate immune sensing by pathogen recognition receptors on DC maturation, HIV infection, and on the quality of HS CTL activation. Remarkably, ligand‐driven triggering of TLR‐3, ‐4, NOD2, and DC‐SIGN, despite reducing viral replication, markedly increased the capacity of infected DCs to stimulate HS CTLs. This was exemplified by the diversity and the quantity of cytokines produced by HS CTLs primed by these DCs. Infecting DCs with viruses harboring members of the APOBEC family of antiviral factors enhanced the antigen‐presenting skills of infected DCs. Our results highlight the tight interplay between innate and adaptive immunity and may help develop innovative immunotherapies against viral infections.