Please use this identifier to cite or link to this item: https://hdl.handle.net/20.500.12530/21905
Title: CD81 controls immunity to Listeria infection through rac-dependent inhibition of proinflammatory mediator release and activation of cytotoxic T cells.
Authors: 
Mesh: 
Issue Date: 15-Jun-2015
Citation: J. Immunol..2015 Jun;(194)12:6090-101
Abstract: Despite recent evidence on the involvement of CD81 in pathogen binding and Ag presentation by dendritic cells (DCs), the molecular mechanism of how CD81 regulates immunity during infection remains to be elucidated. To investigate the role of CD81 in the regulation of defense mechanisms against microbial infections, we have used the Listeria monocytogenes infection model to explore the impact of CD81 deficiency in the innate and adaptive immune response against this pathogenic bacteria. We show that CD81(-/-) mice are less susceptible than wild-type mice to systemic Listeria infection, which correlates with increased numbers of inflammatory monocytes and DCs in CD81(-/-) spleens, the main subsets controlling early bacterial burden. Additionally, our data reveal that CD81 inhibits Rac/STAT-1 activation, leading to a negative regulation of the production of TNF-α and NO by inflammatory DCs and the activation of cytotoxic T cells by splenic CD8α(+) DCs. In conclusion, this study demonstrates that CD81-Rac interaction exerts an important regulatory role on the innate and adaptive immunity against bacterial infection and suggests a role for CD81 in the development of novel therapeutic targets during infectious diseases.
PMID: 25972472
URI: https://hdl.handle.net/20.500.12530/21905
Appears in Collections:Hospitales > H. U. Santa Cristina > Artículos
Fundaciones e Institutos de Investigación > IIS H. U. La Princesa > Artículos

Files in This Item:
The file with the full text of this item is not available due to copyright restrictions or because there is no digital version. Authors can contact the head of the repository of their center to incorporate the corresponding file.


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.