title: TLR4-independent upregulation of activation markers in mouse B lymphocytes infected by HRSV.
abstract: 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.
authors.affiliation: Unidad de Proteómica/Procesamiento Antigénico, Centro Nacional de Microbiología, Instituto de Salud Carlos III, 28220 Majadahonda, Madrid, Spain.
authors.forename: Miguel Angel
authors.initials: MA
authors.lastname: Rico
authors.forename: Susana
authors.initials: S
authors.lastname: Infantes
authors.forename: Manuel
authors.initials: M
authors.lastname: Ramos
authors.forename: Alfonsina
authors.initials: A
authors.lastname: Trento
authors.forename: Carolina
authors.initials: C
authors.lastname: Johnstone
authors.forename: José Antonio
authors.initials: JA
authors.lastname: Melero
authors.forename: Margarita
authors.initials: M
authors.lastname: Del Val
authors.forename: Daniel
authors.initials: D
authors.lastname: López
mesh_terms: D000818:Animals; D001402:B-Lymphocytes / Q000276:immunology* / Q000378:metabolism / Q000821:virology; D051940:B7-2 Antigen / Q000276:immunology / Q000378:metabolism; D002469:Cell Separation; D002478:Cells, Cultured; D005260:Female; D005434:Flow Cytometry; D000949:Histocompatibility Antigens Class II / Q000276:immunology / Q000378:metabolism; D054884:Host-Pathogen Interactions; D006801:Humans; D008213:Lymphocyte Activation / Q000276:immunology*; D051379:Mice; D018345:Mice, Knockout; D018113:Respiratory Syncytial Virus, Human / Q000276:immunology* / Q000502:physiology; D051197:Toll-Like Receptor 4 / Q000235:genetics / Q000276:immunology* / Q000378:metabolism; D015854:Up-Regulation
chemical_list: D051940:B7-2 Antigen; D000949:Histocompatibility Antigens Class II; C493487:Tlr4 protein, mouse; D051197:Toll-Like Receptor 4