Please use this identifier to cite or link to this item:http://hdl.handle.net/20.500.12105/10657
TLR4-independent upregulation of activation markers in mouse B lymphocytes infected by HRSV.
Mol Immunol . 2010 May;47(9):1802-7.
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.
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
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