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  • Title: Interleukin-10-induced HIV-1 expression is mediated by induction of both membrane-bound tumour necrosis factor (TNF)-alpha and TNF receptor type 1 in a promonocytic cell line.
    Author: Barcellini W, Rizzardi GP, Marriott JB, Fain C, Shattock RJ, Meroni PL, Poli G, Dalgleish AG.
    Journal: AIDS; 1996 Jul; 10(8):835-42. PubMed ID: 8828740.
    Abstract:
    OBJECTIVE: To investigate whether the upregulatory effect of interleukin (IL)-10 on HIV expression in a model of latent HIV infection is mediated by induction of endogenous tumour necrosis factor (TNF)-alpha and TNF receptors (TNFR). DESIGN: The latently HIV-infected promonocytic cell line U1 was examined, because in this in vitro model IL-10 has been shown to synergize with multiple cytokines, including TNF-alpha, in enhancing HIV production. METHODS: Membrane-bound TNF-alpha, TNFR-1 and TNFR-2 surface expression were determined by flow cytometry. TNF-alpha mRNA was estimated by competitive polymerase chain reaction (PCR), and TNF-alpha, soluble TNFR-1 and soluble TNFR-2 supernatant content by enzyme-linked immunosorbent assay. HIV-1 expression was quantitated by reverse transcriptase assay and p24 antigen release. RESULTS: We demonstrated that IL-10 induces a time and cell-concentration dependent upregulation of HIV expression in U1 cells. This effect is mediated through the endogenous production of TNF-alpha as demonstrated by blocking experiments with anti-TNF-alpha antibodies and by detection of IL-10-induced increase of TNF-alpha mRNA by competitive PCR. More importantly, IL-10 is able to upregulate membrane-bound TNF-alpha and TNFR-1, along with a consistent increase in the shedding of soluble TNFR-1 without inducing detectable TNF-alpha secretion. CONCLUSIONS: IL-10 activates HIV expression through the membrane-bound TNF-alpha/TNFR-1 pathway, suggesting an amplification mechanism of HIV expression that might occur during cell-to-cell interaction. This positive regulatory effect of IL-10 in an in vitro model of chronic HIV infection is consistent with the inexorable progression of disease seen in advanced patients when both IL-10 and TNF-alpha are elevated.
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