ArticleClinical and diagnostic laboratory immunology1995
Impairment of monocytic function after influenza virus infection.
Article in Clinical and diagnostic laboratory immunology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed, 8 citations in OpenAlex.
- PB1-F2 Protein Does Not Impact the Virulence of Triple-Reassortant H3N2 Swine Influenza Virus in Pigs but Alters Pathogenicity and Transmission in Turkeys.Journal of virology · 2016Article
- Impaired accessory cell function in a human dendritic cell line after human immunodeficiency virus infection.Clinical and diagnostic laboratory immunology · 2005Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
In order to analyze the immunosuppression associated with influenza virus infection, we investigated monocytic function in macrophage hybridoma cell lines 5 weeks after infection with two strains of influenza virus. Clones 30 and 63, chosen for stability in long-term culture, were infected with two strains of influenza virus, X-31 and PR-8. Uniform infection of both cell lines was confirmed by intracytoplasmic staining with the antihemagglutinin strain-specific monoclonal antibodies PY 102 and PY 206. One week after infection, clones 30 and 63 lost their ability to stimulate tetanus toxoid-specific major histocompatibility complex (MHC)-matched responder T cells. Coincident with the inability to stimulate MHC-matched T cells, there was diminished surface expression of class II MHC antigens and LFA-1-alpha and LFA-3 compared with that in uninfected cells: DR, 2.5 versus 10.6% (mean channel 0.3 versus 1.5); DQ, 1.6 versus 15.6% (mean channel 0.3 versus 3.0); DP, 5.0 versus 30.9% (mean channel 0.3 versus 2.0). LFA-1-alpha expression was reduced (13.1 versus 20.0%; mean channel 1.5 versus 2.0) while LFA-3 expression remained the same (22.2 versus 324%; mean channel 3.0 versus 3.3). Class I MHC surface antigen expression was unaltered. Cytokine secretion was also perturbed, as interleukin 1-alpha (IL-1-alpha) and IL-1-beta production was lost 1 week after infection. Production of IL-12 and IL-10 was unchanged, while IL-6 production was increased. The viability of the T cells cocultured with 63Flu was unaltered, demonstrating that the inability of the MHC-restricted T cells to proliferate in response to tetanus toxoid was not due to a toxic effect of 63Flu. Interestingly, other accessory functions, including the ability to support mitogen- and anti-CD3-mediated T-cell proliferation, remained intact. These data suggest that alteration of macrophage function relating to viral infection occurs at multiple levels and may contribute to the immunosuppression observed following influenza virus infection.
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