title: Influenza virus neuraminidase alters allogeneic T cell proliferation.
abstract: Influenza virus elicits good cellular and humoral immune responses. Unlike the cytotoxic T lymphocyte response to many other antigens, the cytotoxic T lymphocyte response to influenza virus is CD4(+) T cell independent, suggesting that viral infection of antigen-presenting cells may alter their capacity to stimulate T cell responses. To clarify the role of influenza virus in these functional alterations, we compared T cell responses to uninfected and A/PR/8/34-infected dendritic cells (DC). DC were prepared from the bone marrow of C57BL/6 (H2(b)) mice and used to stimulate in vivo and in vitro alloreactive T cell responses. In both cases, influenza virus infection increased the capacity of DC to stimulate T cell proliferation. This enhancement was blocked by antibodies specific for neuraminidase (NA), but not hemagglutinin. Infection was not required to observe enhanced T cell proliferation, showing that NA from exogeneous virus particles can facilitate this effect. These results are the first to show that influenza virus alters the capacity of DC to stimulate T cell proliferation through mechanisms mediated by viral NA.
authors.affiliation: Department of International Health, Johns Hopkins University School of Hygiene and Public Health, 615 N. Wolfe Street, Baltimore, Maryland, 21205, USA.
authors.forename: SangKon
authors.initials: S
authors.lastname: Oh
authors.forename: Maryna C
authors.initials: MC
authors.lastname: Eichelberger
mesh_terms: D000818:Animals; D002455:Cell Division; D002460:Cell Line; D002478:Cells, Cultured; D002642:Chick Embryo; D003713:Dendritic Cells / Q000166:cytology / Q000821:virology; D004285:Dogs; D005260:Female; D006801:Humans; D009980:Influenza A virus / Q000201:enzymology* / Q000502:physiology; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D009439:Neuraminidase / Q000378:metabolism*; D013601:T-Lymphocytes / Q000166:cytology* / Q000821:virology
chemical_list: D009439:Neuraminidase