Ligand passing by the p75 tumour necrosis factor receptor enhances HIV-1 activation

S. T. Butera, B. D. Roberts, T. M. Folks

    Research output: Contribution to journalArticlepeer-review

    9 Scopus citations


    Recently, a HIV-dependent upmodulation of the p75 tumour necrosis factor receptor (TNFr75) was observed using latently-infected OM-10.1 promyelocytes; although the participation of TNFr75 in HIV-1 activation remained undefined. Here, using receptor cross-linking by agonistic antibodies, no direct HIV-1 activation via TNFr75 was observed. Signalling via the p55 tumour necrosis factor receptor (TNFr55) accounted for the full extent of HIV-1 activation in OM-10.1 cultures. However, in tumour necrosis factor alpha (TNF-α) dose titration experiments, antibody blockade of TNFr75 decreased the dose response markedly, indicating a ligand passing function. TNFr75 blockade did not alter the dose response to agonistic TNFr55 antibody induction; verifying that the effect on the TNF-α dose response was not due to negative signalling or cytolysis. These results demonstrate that, although not directly involved in signal transduction resulting in HIV-1 activation, TNFr75 can serve a critical ligand passing function and permit continued HIV-1 expression during limited TNF-α availability.

    Original languageEnglish (US)
    Pages (from-to)745-750
    Number of pages6
    Issue number10
    StatePublished - Oct 1996


    • Agonistic antibody
    • HIV expression
    • Ligand passing
    • TNF receptor

    ASJC Scopus subject areas

    • Immunology and Allergy
    • Immunology
    • Biochemistry
    • Hematology
    • Molecular Biology


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