Poly(I:C) promotes the production of IL‐17A by murine CD1d‐driven invariant NKT cells in airway inflammation
Identifieur interne : 001361 ( Main/Exploration ); précédent : 001360; suivant : 001362Poly(I:C) promotes the production of IL‐17A by murine CD1d‐driven invariant NKT cells in airway inflammation
Auteurs : A. Vultaggio [Italie] ; F. Nencini [Italie] ; S. Pratesi [Italie] ; G. Petroni [Italie] ; S. Romagnani [Italie] ; E. Maggi [Italie]Source :
- Allergy [ 0105-4538 ] ; 2012-10.
English descriptors
- Teeft :
- Agonist, Airway, Airway hyperreactivity, Allergy, Allergy clin immunol, Asthma, Balf, Bmdc, Culture supernatants, Cytokine, Dendritic cells, Elisa, Galcer, Galcer polydta, Immunol, Inkt, Inkt cell subset, Inkt cells, Isotype, Isotype control, Isotype control mabs, John wiley sons, John wiley sons tlr3 agonist lung inkt cells vultaggio, Mabs, Mrna, Mrna expression, Murine, Neutralizing, Neutrophil, Polydta, Receptor, Right panel, Separate experiments, Serum levels, Spleen, Spleen cells, Subset, Supernatant, Tlr3, Tlr3 agonist lung inkt cells, Tlr7, Tlr7 agonists, Viral, Viral infections, Vultaggio.
Abstract
Background: IL‐17A is associated with different asthma phenotypes as virus‐associated or steroid‐resistant asthma. Invariant natural killer T (iNKT) cells play an important role in the pathogenesis of asthma. The aim of the study was to evaluate the activity of polyinosinic–polycytidylic acid [poly(I:C)] on IL‐17A production by CD1d‐activated iNKT cells. Methods: We analysed the in vitro effect of poly(I:C) on the release of IL‐17A by spleen and lung CD1d‐activated iNKT cells with α‐galactosylceramide (α‐GalCer). Its activity was also investigated in an α‐GalCer‐induced murine models, including lung inflammation. The inhibition of IL‐17A by Toll‐like receptor (TLR) 7 agonists in the same in vitro and in vivo models has been analysed. Results: Poly(I:C) upregulated the in vitro IL‐17A production by CD1d‐activated NK1.1− CD4− iNKT subset, without modifying type 1 and type 2 cytokines. The two stimuli selectively upregulated IL‐17A serum levels in vivo. Their intratracheal administration resulted in increased airway hyper‐reactivity (AHR), neutrophilia in bronchoalveolar lavage and airway inflammation, which were inhibited by anti‐IL‐17A antibody. Poly(I:C) effects were attributable to IL1β and IL‐23 release from dendritic cells, as showed by inhibition with neutralizing antibodies. TLR7 agonists inhibited the IL‐17A production by poly(I:C) plus α‐GalCer in the same models. Such effect was associated with the increased production by DC of IL‐17A‐inhibiting cytokines and the dampening of IL‐1β and IL‐23. Conclusions: Synthetic dsRNA selectively expand a CD1d‐driven IL‐17A‐producing iNKT cell subset, thus explaining the worsening of airway inflammation by some viral infections. TLR3‐ and TLR7‐triggering viral sequences can exert variable and opposite effects on adaptive immune response.
Url:
DOI: 10.1111/j.1398-9995.2012.02876.x.
Affiliations:
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Romagnani</name><affiliation wicri:level="1"><country xml:lang="fr">Italie</country><wicri:regionArea>Centre of Research, Transfer and High Education DENOTHE, University of Florence, Florence</wicri:regionArea><wicri:noRegion>Florence</wicri:noRegion></affiliation><affiliation wicri:level="1"><country xml:lang="fr">Italie</country><wicri:regionArea>Department of Internal Medicine, University of Florence, Florence</wicri:regionArea><wicri:noRegion>Florence</wicri:noRegion></affiliation></author><author><name sortKey="Maggi, E" sort="Maggi, E" uniqKey="Maggi E" first="E." last="Maggi">E. Maggi</name><affiliation wicri:level="1"><country xml:lang="fr">Italie</country><wicri:regionArea>Centre of Research, Transfer and High Education DENOTHE, University of Florence, Florence</wicri:regionArea><wicri:noRegion>Florence</wicri:noRegion></affiliation><affiliation wicri:level="1"><country xml:lang="fr">Italie</country><wicri:regionArea>Department of Internal Medicine, University of Florence, Florence</wicri:regionArea><wicri:noRegion>Florence</wicri:noRegion></affiliation><affiliation></affiliation><affiliation wicri:level="1"><country wicri:rule="url">Italie</country></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Allergy</title><title level="j" type="alt">ALLERGY</title><idno type="ISSN">0105-4538</idno><idno type="eISSN">1398-9995</idno><imprint><biblScope unit="vol">67</biblScope><biblScope unit="issue">10</biblScope><biblScope unit="page" from="1223">1223</biblScope><biblScope unit="page" to="1232">1232</biblScope><biblScope unit="page-count">10</biblScope><date type="published" when="2012-10">2012-10</date></imprint><idno type="ISSN">0105-4538</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0105-4538</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Agonist</term><term>Airway</term><term>Airway hyperreactivity</term><term>Allergy</term><term>Allergy clin immunol</term><term>Asthma</term><term>Balf</term><term>Bmdc</term><term>Culture supernatants</term><term>Cytokine</term><term>Dendritic cells</term><term>Elisa</term><term>Galcer</term><term>Galcer polydta</term><term>Immunol</term><term>Inkt</term><term>Inkt cell subset</term><term>Inkt cells</term><term>Isotype</term><term>Isotype control</term><term>Isotype control mabs</term><term>John wiley sons</term><term>John wiley sons tlr3 agonist lung inkt cells vultaggio</term><term>Mabs</term><term>Mrna</term><term>Mrna expression</term><term>Murine</term><term>Neutralizing</term><term>Neutrophil</term><term>Polydta</term><term>Receptor</term><term>Right panel</term><term>Separate experiments</term><term>Serum levels</term><term>Spleen</term><term>Spleen cells</term><term>Subset</term><term>Supernatant</term><term>Tlr3</term><term>Tlr3 agonist lung inkt cells</term><term>Tlr7</term><term>Tlr7 agonists</term><term>Viral</term><term>Viral infections</term><term>Vultaggio</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract">Background: IL‐17A is associated with different asthma phenotypes as virus‐associated or steroid‐resistant asthma. Invariant natural killer T (iNKT) cells play an important role in the pathogenesis of asthma. The aim of the study was to evaluate the activity of polyinosinic–polycytidylic acid [poly(I:C)] on IL‐17A production by CD1d‐activated iNKT cells. Methods: We analysed the in vitro effect of poly(I:C) on the release of IL‐17A by spleen and lung CD1d‐activated iNKT cells with α‐galactosylceramide (α‐GalCer). Its activity was also investigated in an α‐GalCer‐induced murine models, including lung inflammation. The inhibition of IL‐17A by Toll‐like receptor (TLR) 7 agonists in the same in vitro and in vivo models has been analysed. Results: Poly(I:C) upregulated the in vitro IL‐17A production by CD1d‐activated NK1.1− CD4− iNKT subset, without modifying type 1 and type 2 cytokines. The two stimuli selectively upregulated IL‐17A serum levels in vivo. Their intratracheal administration resulted in increased airway hyper‐reactivity (AHR), neutrophilia in bronchoalveolar lavage and airway inflammation, which were inhibited by anti‐IL‐17A antibody. Poly(I:C) effects were attributable to IL1β and IL‐23 release from dendritic cells, as showed by inhibition with neutralizing antibodies. TLR7 agonists inhibited the IL‐17A production by poly(I:C) plus α‐GalCer in the same models. Such effect was associated with the increased production by DC of IL‐17A‐inhibiting cytokines and the dampening of IL‐1β and IL‐23. Conclusions: Synthetic dsRNA selectively expand a CD1d‐driven IL‐17A‐producing iNKT cell subset, thus explaining the worsening of airway inflammation by some viral infections. TLR3‐ and TLR7‐triggering viral sequences can exert variable and opposite effects on adaptive immune response.</div></front></TEI><affiliations><list><country><li>Italie</li></country></list><tree><country name="Italie"><noRegion><name sortKey="Vultaggio, A" sort="Vultaggio, A" uniqKey="Vultaggio A" first="A." last="Vultaggio">A. Vultaggio</name></noRegion><name sortKey="Maggi, E" sort="Maggi, E" uniqKey="Maggi E" first="E." last="Maggi">E. Maggi</name><name sortKey="Maggi, E" sort="Maggi, E" uniqKey="Maggi E" first="E." last="Maggi">E. Maggi</name><name sortKey="Maggi, E" sort="Maggi, E" uniqKey="Maggi E" first="E." last="Maggi">E. Maggi</name><name sortKey="Nencini, F" sort="Nencini, F" uniqKey="Nencini F" first="F." last="Nencini">F. Nencini</name><name sortKey="Nencini, F" sort="Nencini, F" uniqKey="Nencini F" first="F." last="Nencini">F. Nencini</name><name sortKey="Petroni, G" sort="Petroni, G" uniqKey="Petroni G" first="G." last="Petroni">G. Petroni</name><name sortKey="Petroni, G" sort="Petroni, G" uniqKey="Petroni G" first="G." last="Petroni">G. Petroni</name><name sortKey="Pratesi, S" sort="Pratesi, S" uniqKey="Pratesi S" first="S." last="Pratesi">S. Pratesi</name><name sortKey="Pratesi, S" sort="Pratesi, S" uniqKey="Pratesi S" first="S." last="Pratesi">S. Pratesi</name><name sortKey="Romagnani, S" sort="Romagnani, S" uniqKey="Romagnani S" first="S." last="Romagnani">S. Romagnani</name><name sortKey="Romagnani, S" sort="Romagnani, S" uniqKey="Romagnani S" first="S." last="Romagnani">S. Romagnani</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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