Por favor, use este identificador para citar o enlazar este Item:http://hdl.handle.net/20.500.12105/10657
Título
TLR4-independent upregulation of activation markers in mouse B lymphocytes infected by HRSV.
Autor(es)
Rico, Miguel Angel | Trento, Alfonsina ISCIII | Melero, Jose Antonio ISCIII | Infantes, Susana ISCIII | Ramos, Manuel ISCIII | Johnstone, Carolina ISCIII | Val, Margarita del | Lopez, Daniel ISCIII
Fecha de publicación
2010-05
Cita
Mol Immunol . 2010 May;47(9):1802-7.
Idioma
Inglés
Tipo de documento
journal article
Resumen
Human respiratory syncytial virus (HRSV) is the most common cause of severe respiratory infections in infants and young children, often leading to hospitalization. In addition, HRSV poses a serious health risk in immunocompromised individuals and the elderly. It has been reported that this virus can infect mouse antigen-presenting cells, including B lymphocytes. In these B cells, HRSV infection upregulates the expression of activation markers, including MHC class II and CD86, but not MHC class I molecules. Here, we report that HRSV infection of spleen B lymphocytes downregulated TLR4. Either blocking with anti-TLR4 antibody or genetic deletion, but not functional deficiency of TLR4, moderately reduced the infectivity of HRSV in B lymphocytes. HRSV-infected B lymphocytes with deleted TLR4 upregulated MHC class II and CD86 molecules to the same levels as TLR4(+) wild type B cells. Since the activation of monocytes and macrophages by HRSV was previously reported to depend on TLR4, the current study indicates that these cells and B lymphocytes respond to HRSV infection with different activation pathways.
MESH
Animals | B-Lymphocytes | B7-2 Antigen | Cell Separation | Cells, Cultured | Female | Flow Cytometry | Histocompatibility Antigens Class II | Host-Pathogen Interactions | Humans | Lymphocyte Activation | Mice | Mice, Knockout | Respiratory Syncytial Virus, Human | Toll-Like Receptor 4 | Up-Regulation
Versión en línea
DOI
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