title: Plasmacytoid dendritic cells are dispensable during primary influenza virus infection.
abstract: Plasmacytoid dendritic cells (pDC) are thought to be pivotal in the first line of defense against viral infections. Although previous studies have suggested that pDC regulate the immune response against respiratory syncytial virus, their role in pulmonary infection with influenza virus has remained unclear. Using mice with GFP-tagged pDC, we observed a marked increase in pDC numbers in the lung airways 3 days after intranasal infection with influenza virus A/PR/8/34. To further investigate their potential involvement in the disease, we made use of pDC-deficient IkarosL/L mice. In the absence of pDC, the recruitment of T cells to the bronchoalveolar space was delayed, which could be reversed by the adoptive transfer of pDC before infection. Surprisingly, however, when compared with wild-type animals, IkarosL/L mice revealed a similar course of disease, as determined by weight loss, viral titers, levels of neutralizing Ab, and lung pathology. Moreover, the activation and differentiation of influenza-specific CD8+ effector T cells was unaltered in the absence of pDC, as was the generation of CD8+ memory T cells. Taken together, our study suggests that pDC regulate the accumulation of T cells in the bronchoalveolar space during early influenza virus infection, but are dispensable for the control of this disease.
authors.affiliation: Immunology Program, The Wistar Institute, Philadelphia, PA 19104, USA.
authors.forename: Amaya I
authors.initials: AI
authors.lastname: Wolf
authors.forename: Darya
authors.initials: D
authors.lastname: Buehler
authors.forename: Scott E
authors.initials: SE
authors.lastname: Hensley
authors.forename: Lois L
authors.initials: LL
authors.lastname: Cavanagh
authors.forename: E John
authors.initials: EJ
authors.lastname: Wherry
authors.forename: Philippe
authors.initials: P
authors.lastname: Kastner
authors.forename: Susan
authors.initials: S
authors.lastname: Chan
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Weninger
mesh_terms: D000818:Animals; D001402:B-Lymphocytes / Q000276:immunology / Q000473:pathology; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology / Q000276:immunology / Q000821:virology; D002454:Cell Differentiation / Q000235:genetics / Q000276:immunology; D045744:Cell Line, Tumor; D019070:Cell Lineage / Q000235:genetics / Q000276:immunology; D002465:Cell Movement / Q000276:immunology*; D003713:Dendritic Cells / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D051740:Ikaros Transcription Factor / Q000235:genetics; D053118:Influenza A Virus, H1N1 Subtype / Q000276:immunology*; D007962:Leukocytes / Q000276:immunology / Q000473:pathology; D008168:Lung / Q000276:immunology / Q000473:pathology / Q000821:virology; D008546:Melanoma, Experimental / Q000276:immunology / Q000473:pathology; D051379:Mice; D018345:Mice, Knockout; D008822:Mice, Transgenic; D009976:Orthomyxoviridae Infections / Q000276:immunology* / Q000473:pathology; D012141:Respiratory Tract Infections / Q000276:immunology* / Q000473:pathology; D013601:T-Lymphocytes / Q000276:immunology / Q000821:virology
chemical_list: C497238:Zfpn1a1 protein, mouse; D051740:Ikaros Transcription Factor