Abstract
Similarly to HIV-infected cells, recombinant HIV-1 glycoprotein 120 induces acid-labile interferon production in peripheral blood mononuclear cells from healthy donors. Acid lability of this interferon is due to the presence of both IFN-α and -γ molecules. In fact, although not revealed by neutralization of antiviral activity with antibody to IFN-γ, the presence of IFN-γ was shown both immunoenzymatically and by detection of specific mRNA in gp120-stimulated cells. The source of IFN-γ appears to be a T cell present in the CD4-enriched subpopulation. Cultures treated with monoclonal antibodies to the ICAM-1 and LFA-1 adhesion molecules showed an impaired release of both IFN types after gp120 stimulation, suggesting a crucial role of cell-to-cell interactions in the process leading to IFN production. Our data suggest that the HIV envelope glycoprotein could be responsible for the induction of endogenous IFN-α and -γ observed in AIDS patients.
| Original language | English |
|---|---|
| Pages (from-to) | 957-962 |
| Number of pages | 6 |
| Journal | AIDS Research and Human Retroviruses |
| Volume | 9 |
| Issue number | 10 |
| Publication status | Published - 1993 |
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ASJC Scopus subject areas
- Immunology
- Virology
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Coordinate induction of interferon α and γ by recombinant HIV-1 glycoprotein 120. / Capobianchi, M. R.; Ameglio, F.; Fei, P. C.; Castilletti, C.; Mercuri, F.; Fais, S.; Dianzani, F.
In: AIDS Research and Human Retroviruses, Vol. 9, No. 10, 1993, p. 957-962.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Coordinate induction of interferon α and γ by recombinant HIV-1 glycoprotein 120
AU - Capobianchi, M. R.
AU - Ameglio, F.
AU - Fei, P. C.
AU - Castilletti, C.
AU - Mercuri, F.
AU - Fais, S.
AU - Dianzani, F.
PY - 1993
Y1 - 1993
N2 - Similarly to HIV-infected cells, recombinant HIV-1 glycoprotein 120 induces acid-labile interferon production in peripheral blood mononuclear cells from healthy donors. Acid lability of this interferon is due to the presence of both IFN-α and -γ molecules. In fact, although not revealed by neutralization of antiviral activity with antibody to IFN-γ, the presence of IFN-γ was shown both immunoenzymatically and by detection of specific mRNA in gp120-stimulated cells. The source of IFN-γ appears to be a T cell present in the CD4-enriched subpopulation. Cultures treated with monoclonal antibodies to the ICAM-1 and LFA-1 adhesion molecules showed an impaired release of both IFN types after gp120 stimulation, suggesting a crucial role of cell-to-cell interactions in the process leading to IFN production. Our data suggest that the HIV envelope glycoprotein could be responsible for the induction of endogenous IFN-α and -γ observed in AIDS patients.
AB - Similarly to HIV-infected cells, recombinant HIV-1 glycoprotein 120 induces acid-labile interferon production in peripheral blood mononuclear cells from healthy donors. Acid lability of this interferon is due to the presence of both IFN-α and -γ molecules. In fact, although not revealed by neutralization of antiviral activity with antibody to IFN-γ, the presence of IFN-γ was shown both immunoenzymatically and by detection of specific mRNA in gp120-stimulated cells. The source of IFN-γ appears to be a T cell present in the CD4-enriched subpopulation. Cultures treated with monoclonal antibodies to the ICAM-1 and LFA-1 adhesion molecules showed an impaired release of both IFN types after gp120 stimulation, suggesting a crucial role of cell-to-cell interactions in the process leading to IFN production. Our data suggest that the HIV envelope glycoprotein could be responsible for the induction of endogenous IFN-α and -γ observed in AIDS patients.
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M3 - Article
C2 - 7904170
AN - SCOPUS:0027135736
VL - 9
SP - 957
EP - 962
JO - AIDS Research and Human Retroviruses
JF - AIDS Research and Human Retroviruses
SN - 0889-2229
IS - 10
ER -