NFκB activation by modified vaccinia virus as a novel strategy to enhance neutrophil migration and HIV-specific T-cell responses.

Détails

ID Serval
serval:BIB_C6CDF3DAF499
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
NFκB activation by modified vaccinia virus as a novel strategy to enhance neutrophil migration and HIV-specific T-cell responses.
Périodique
Proceedings of the National Academy of Sciences of the United States of America
Auteur(s)
Di Pilato M., Mejías-Pérez E., Zonca M., Perdiguero B., Gómez C.E., Trakala M., Nieto J., Nájera J.L., S Sorzano C.O., Combadière C., Pantaleo G., Planelles L., Esteban M.
ISSN
1091-6490 (Electronic)
ISSN-L
0027-8424
Statut éditorial
Publié
Date de publication
2015
Peer-reviewed
Oui
Volume
112
Numéro
11
Pages
E1333-E1342
Langue
anglais
Notes
Publication types: Journal Article Publication Status: ppublish
Résumé
Neutrophils are antigen-transporting cells that generate vaccinia virus (VACV)-specific T-cell responses, yet how VACV modulates neutrophil recruitment and its significance in the immune response are unknown. We generated an attenuated VACV strain that expresses HIV-1 clade C antigens but lacks three specific viral genes (A52R, K7R, and B15R). We found that these genes act together to inhibit the NFκB signaling pathway. Triple ablation in modified virus restored NFκB function in macrophages. After virus infection of mice, NFκB pathway activation led to expression of several cytokines/chemokines that increased the migration of neutrophil populations (Nα and Nβ) to the infection site. Nβ cells displayed features of antigen-presenting cells and activated virus-specific CD8 T cells. Enhanced neutrophil trafficking to the infection site correlated with an increased T-cell response to HIV vector-delivered antigens. These results identify a mechanism for poxvirus-induced immune response and alternatives for vaccine vector design.
Pubmed
Web of science
Open Access
Oui
Création de la notice
10/04/2015 19:13
Dernière modification de la notice
09/05/2019 1:04
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