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Clinical and Diagnostic Laboratory Immunology, Jul 1995, 426-433, Vol 2, No. 4
Copyright © 1995 by the American Society for Microbiology. All rights reserved.

Impairment of monocytic function after influenza virus infection

M Louie, J Yoo, T Moran, L Mayer and K Sperber
Division of Clinical Immunology, Mount Sinai Medical Center, New York 10029, USA.

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.(ABSTRACT TRUNCATED AT 250 WORDS)

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