FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W4313311491> ?p ?o ?g. }

• W4313311491 endingPage "263" @default.
• W4313311491 startingPage "256" @default.
• W4313311491 abstract "Abstract To investigate the defensive roles and production of interferon and antibodies, C3H/He mice were subjected to various immunosuppressive treatments and infected with influenza virus. In infected normal control mice the pattern of pulmonary viral growth can be divided into three phases. The first phase is characterized by an exponential increase of virus titer, the second by a rapid decrease, and the third by a moderate decrease. At the time of transition from the first phase to the second in pulmonary virus growth, interferon could be detected in the tracheobronchial washings of infected mice, but neutralizing antibodies could not. In infected B cell-deprived mice and infected anti-µ-treated mice, the transition from the first phase to the second occurred without any detectable antibody production, and interferon could be induced in the early stage of infection. However, the pulmonary virus in these mice increased again exponentially until the death of the mice. In infected T cell-deprived mice which could not induce interferon, but produced IgM-neutralizing antibodies, the second phase was not observed after the first phase, but a transient plateau phase could be demonstrated, and then the pulmonary virus increased again exponentially until the death of the mice. In anti-γ-treated infected mice, pulmonary virus growth and production of interferon and neutralizing antibody were almost similar to those of infected normal control mice except for the absence of IgG neutralizing antibody production. Although anti-α-treated infected mice produced interferon and no IgA antibody, the transition from the first exponential increase of pulmonary virus to the second rapid decrease was seen, but then the virus increased exponentially again until the death of the mice. These results suggest that interferon plays an important role in the transition from the first phase to the second, and that T cells are required for interferon induction in mice infected with influenza virus. These data also suggest that IgA antibodies play an important role in the inhibition of virus propagation in the lungs after the disappearance of interferon. Moreover, infected T cell-deprived mice could produce only IgM neutralizing antibodies, but not IgG and IgA antibodies. Therefore, T cells are required for the production of IgG and IgA antibodies and eventually for defense functions in mice infected primarily with influenza virus." @default.
• W4313311491 created "2023-01-06" @default.
• W4313311491 creator A5015522425 @default.
• W4313311491 creator A5073139809 @default.
• W4313311491 date "1977-01-01" @default.
• W4313311491 modified "2023-10-16" @default.
• W4313311491 title "Defense Mechanisms Against Primary Influenza Virus Infection in Mice" @default.
• W4313311491 doi "https://doi.org/10.4049/jimmunol.118.1.256" @default.
• W4313311491 hasPublicationYear "1977" @default.
• W4313311491 type Work @default.
• W4313311491 citedByCount "29" @default.
• W4313311491 countsByYear W43133114912012 @default.
• W4313311491 countsByYear W43133114912013 @default.
• W4313311491 countsByYear W43133114912014 @default.
• W4313311491 countsByYear W43133114912017 @default.
• W4313311491 countsByYear W43133114912021 @default.
• W4313311491 countsByYear W43133114912023 @default.
• W4313311491 crossrefType "journal-article" @default.
• W4313311491 hasAuthorship W4313311491A5015522425 @default.
• W4313311491 hasAuthorship W4313311491A5073139809 @default.
• W4313311491 hasBestOaLocation W43133114911 @default.
• W4313311491 hasConcept C159047783 @default.
• W4313311491 hasConcept C159654299 @default.
• W4313311491 hasConcept C203014093 @default.
• W4313311491 hasConcept C2522874641 @default.
• W4313311491 hasConcept C2776178377 @default.
• W4313311491 hasConcept C2779261636 @default.
• W4313311491 hasConcept C32611913 @default.
• W4313311491 hasConcept C86803240 @default.
• W4313311491 hasConceptScore W4313311491C159047783 @default.
• W4313311491 hasConceptScore W4313311491C159654299 @default.
• W4313311491 hasConceptScore W4313311491C203014093 @default.
• W4313311491 hasConceptScore W4313311491C2522874641 @default.
• W4313311491 hasConceptScore W4313311491C2776178377 @default.
• W4313311491 hasConceptScore W4313311491C2779261636 @default.
• W4313311491 hasConceptScore W4313311491C32611913 @default.
• W4313311491 hasConceptScore W4313311491C86803240 @default.
• W4313311491 hasIssue "1" @default.
• W4313311491 hasLocation W43133114911 @default.
• W4313311491 hasOpenAccess W4313311491 @default.
• W4313311491 hasPrimaryLocation W43133114911 @default.
• W4313311491 hasRelatedWork W1520753096 @default.
• W4313311491 hasRelatedWork W1693544388 @default.
• W4313311491 hasRelatedWork W1972745941 @default.
• W4313311491 hasRelatedWork W1984647379 @default.
• W4313311491 hasRelatedWork W2022712590 @default.
• W4313311491 hasRelatedWork W2070480238 @default.
• W4313311491 hasRelatedWork W2090002905 @default.
• W4313311491 hasRelatedWork W2093510980 @default.
• W4313311491 hasRelatedWork W2139983200 @default.
• W4313311491 hasRelatedWork W2350366197 @default.
• W4313311491 hasVolume "118" @default.
• W4313311491 isParatext "false" @default.
• W4313311491 isRetracted "false" @default.
• W4313311491 workType "article" @default.