| First Author | Rico MA | Year | 2010 |
| Journal | Mol Immunol | Volume | 47 |
| Issue | 9 | Pages | 1802-7 |
| PubMed ID | 20362337 | Mgi Jnum | J:160628 |
| Mgi Id | MGI:4454739 | Doi | 10.1016/j.molimm.2010.02.019 |
| Citation | Rico MA, et al. (2010) TLR4-independent upregulation of activation markers in mouse B lymphocytes infected by HRSV. Mol Immunol 47(9):1802-7 |
| abstractText | 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. |
