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Bordetella Adenylate Cyclase Toxin Differentially Modulates Toll-Like Receptor-Stimulated Activation, Migration and T Cell Stimulatory Capacity of Dendritic Cells
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SYSNO ASEP 0435908 Document Type J - Journal Article R&D Document Type Journal Article Subsidiary J Článek ve WOS Title Bordetella Adenylate Cyclase Toxin Differentially Modulates Toll-Like Receptor-Stimulated Activation, Migration and T Cell Stimulatory Capacity of Dendritic Cells Author(s) Adkins, Irena (MBU-M)
Kamanová, Jana (MBU-M) ORCID, RID
Kocourková, A. (CZ)
Švédová, Martina (MBU-M)
Tomala, Jakub (MBU-M) RID, ORCID
Janová, H. (CZ)
Mašín, Jiří (MBU-M) RID, ORCID
Chládková, Barbara (MBU-M) RID
Bumba, Ladislav (MBU-M) RID, ORCID
Kovář, Marek (MBU-M) RID, ORCID
Ross, P. J. (IE)
Tučková, Ludmila (MBU-M) RID
Spíšek, R. (CZ)
Mills, K. H. G. (IE)
Šebo, Peter (MBU-M) RID, ORCIDSource Title PLoS ONE. - : Public Library of Science - ISSN 1932-6203
Roč. 9, č. 8 (2014)Number of pages 13 s. Language eng - English Country US - United States Keywords RESPIRATORY-INFECTION ; INTERLEUKIN-10 PRODUCTION ; PROTECTIVE IMMUNITY Subject RIV EE - Microbiology, Virology R&D Projects GA310/08/0447 GA ČR - Czech Science Foundation (CSF) GP310/09/P582 GA ČR - Czech Science Foundation (CSF) GAP301/11/0325 GA ČR - Czech Science Foundation (CSF) 1M0506 GA MŠMT - Ministry of Education, Youth and Sports (MEYS) Institutional support MBU-M - RVO:61388971 UT WOS 000339819800123 DOI 10.1371/journal.pone.0104064 Annotation Adenylate cyclase toxin (CyaA) is a key virulence factor of the whooping cough agent Bordetella pertussis. The toxin targets CD11b-expressing phagocytes and delivers into their cytosol an adenylyl cyclase (AC) enzyme that subverts cellular signaling by increasing cAMP levels. In the present study, we analyzed the modulatory effects of CyaA on adhesive, migratory and antigen presenting properties of Toll-like receptor (TLR)-activated murine and human dendritic cells (DCs). cAMP signaling of CyaA enhanced TLR-induced dissolution of cell adhesive contacts and migration of DCs towards the lymph node-homing chemokines CCL19 and CCL21 in vitro. Moreover, we examined in detail the capacity of toxin-treated DCs to induce CD4(+) and CD8(+) T cell responses. Exposure to CyaA decreased the capacity of LPS-stimulated DCs to present soluble protein antigen to CD4(+) T cells independently of modulation of co-stimulatory molecules and cytokine production, and enhanced their capacity to promote CD4(+) CD25(+) Foxp3(+) T regulatory cells in vitro. In addition, CyaA decreased the capacity of LPS-stimulated DCs to induce CD8(+) T cell proliferation and limited the induction of IFN-gamma producing CD8(+) T cells while enhancing IL-10 and IL-17-production. These results indicate that through activation of cAMP signaling, the CyaA may be mobilizing DCs impaired in T cell stimulatory capacity and arrival of such DCs into draining lymph nodes may than contribute to delay and subversion of host immune responses during B. pertussis infection Workplace Institute of Microbiology Contact Eliška Spurná, eliska.spurna@biomed.cas.cz, Tel.: 241 062 231 Year of Publishing 2015
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