TY - JOUR
T1 - Influenza virus neuraminidase alters aiiogeneic T cell proliferation
AU - Oh, Sangkon
AU - Eichelberger, Maryna C.
N1 - Funding Information:
This work was supported by Grant AI 40489 from NIH. SangKon Oh was supported in part by a student scholarship from the Department of International Health, Johns Hopkins University. We thank Elivia Ramirez and Tricia Nills from the laboratory of Dr. Joe Margolick (Department of Molecular Microbiology and Immunology, Johns Hopkins School of Public Health) for analysis of samples by flow cytometry. We also thank Drs. Robert Webster, Chris Karp, and Nate Pierce for valuable discussions and suggestions.
PY - 1999/11/25
Y1 - 1999/11/25
N2 - 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 (H2b) 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.
AB - 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 (H2b) 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.
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U2 - 10.1006/viro.1999.0019
DO - 10.1006/viro.1999.0019
M3 - Article
C2 - 10562504
AN - SCOPUS:0033604581
SN - 0042-6822
VL - 264
SP - 427
EP - 435
JO - Virology
JF - Virology
IS - 2
ER -