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Tytuł:
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Helicobacter pylori induces activation of human peripheral γδ+ T lymphocytes.
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Autorzy:
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Romi B; Novartis Vaccines and Diagnostics Research Center, Siena, Italy.
Soldaini E
Pancotto L
Castellino F
Del Giudice G
Schiavetti F
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Źródło:
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PloS one [PLoS One] 2011 Apr 29; Vol. 6 (4), pp. e19324. Date of Electronic Publication: 2011 Apr 29.
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Typ publikacji:
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Journal Article
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Język:
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English
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Imprint Name(s):
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Original Publication: San Francisco, CA : Public Library of Science
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MeSH Terms:
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CD3 Complex/*metabolism
Helicobacter Infections/*blood
Helicobacter pylori/*metabolism
Receptors, Antigen, T-Cell, gamma-delta/*metabolism
T-Lymphocytes/*metabolism
T-Lymphocytes/*microbiology
Coculture Techniques ; Flow Cytometry ; Green Fluorescent Proteins/metabolism ; Humans ; Lymphocyte Activation ; Microscopy, Confocal/methods ; Receptors, Antigen, T-Cell/metabolism ; Risk Factors
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References:
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Substance Nomenclature:
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0 (CD3 Complex)
0 (Receptors, Antigen, T-Cell)
0 (Receptors, Antigen, T-Cell, gamma-delta)
147336-22-9 (Green Fluorescent Proteins)
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Entry Date(s):
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Date Created: 20110512 Date Completed: 20111128 Latest Revision: 20211020
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Update Code:
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20240104
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PubMed Central ID:
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PMC3084806
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DOI:
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10.1371/journal.pone.0019324
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PMID:
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21559446
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Helicobacter pylori is a gram-negative bacterium that causes gastric and duodenal diseases in humans. Despite a robust antibody and cellular immune response, H. pylori infection persists chronically. To understand if and how H. pylori could modulate T cell activation, in the present study we investigated in vitro the interaction between H. pylori and human T lymphocytes freshly isolated from peripheral blood of H. pylori-negative donors. A direct interaction of live, but not killed bacteria with purified CD3+ T lymphocytes was observed by microscopy and confirmed by flow cytometry. Live H. pylori activated CD3+ T lymphocytes and predominantly γδ+ T cells bearing the TCR chain Vδ2. Upon interaction with H. pylori, these cells up-regulated the activation molecule CD69 and produced cytokines (such as TNFα, IFNγ) and chemokines (such as MIP-1β, RANTES) in a non-antigen-specific manner. This activation required viable H. pylori and was not exhibited by other gram-negative bacteria. The cytotoxin-associated antigen-A (CagA), was at least partially responsible of this activation. Our results suggest that H. pylori can directly interact with T cells and modulate the response of γδ+ T cells, thereby favouring an inflammatory environment which can contribute to the chronic persistence of the bacteria and eventually to the gastric pathology.