Rico, Miguel AngelTrento, AlfonsinaMelero, Jose AntonioInfantes, SusanaRamos, ManuelJohnstone, CarolinaVal, Margarita delLopez, Daniel2020-07-062020-07-062010-05Mol Immunol . 2010 May;47(9):1802-7.0161-5890http://hdl.handle.net/20.500.12105/10657Human 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.engAMhttp://creativecommons.org/licenses/by-nc-nd/4.0/AnimalsB-LymphocytesB7-2 AntigenCell SeparationCells, CulturedFemaleFlow CytometryHistocompatibility Antigens Class IIHost-Pathogen InteractionsHumansLymphocyte ActivationMiceMice, KnockoutRespiratory Syncytial Virus, HumanToll-Like Receptor 4Up-RegulationAttribution-NonCommercial-NoDerivatives 4.0 Internacional203623374791802-710.1016/j.molimm.2010.02.0191872-9142Molecular immunologyopen access