PubMed · 8153874
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K A Davies, J A Schifferli, M J Walport. 1994. Complement deficiency and immune complex disease.. https://doi.org/10.1007/bf01837367
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HIV-1-infected quiescent CD4+ cells harbor the virus in an inactive state until subsequent activation. The possibility that HIV-1 itself and the virus envelope glycoprotein 120 (gp120) might be important agents of this activation was investigated. The present data indicate that binding of heat-inactivated HIV-1 (iHIV-1) to infected resting PBMCs was sufficient to activate NF-kappa B and AP-1, to induce transition from the G0/G1 stage of the cell cycle to the S/G2/M stage, to induce cell surface expression of CD25, to stimulate provirus integration, and to commit cells to produce virus. The cumulative amount of HIV-1 produced by iHIV-1-stimulated cells strictly depended on the concentration of p24gag in the virion preparations used for stimulation. Moreover, virus production was not evidenced in infected resting cells exposed to iHIV-1 previously incubated with soluble CD4 (sCD4), indicating that activation requires a contact between HIV-1 envelope glycoproteins and cell surface CD4. Although soluble gp120 did not stimulate virus production, we found that transition to the S/G2/M stage of the cell cycle, cell surface expression of activation Ags, and virus production were stimulated by cross-linking of CD4 by gp120-anti-gp120 immune complexes. Finally, incubation of gp120-anti-gp120 immune complexes with sCD4 inhibited these effects. These findings suggest that virions and gp120 anti-gp120 immune complexes found in infected patients at all times of infection can stimulate virus production in CD4+ cells harboring HIV-1 in an inducible state.
The ability of Fc gamma R on monocytes and macrophages to enhance presentation of Ab-bound Ag has been well established. In contrast, studies suggest that Fc gamma RII on B cells functions primarily to suppress B cell responses. We found that presentation of tetanus toxoid (TT) by human EBV-transformed B cells was enhanced by 100- to 1000-fold, when TT was targeted to Fc gamma RII on B cells by using a conjugate consisting of TT covalently linked to anti-human Fc gamma RII mAb 41H16. This enhanced presentation could be blocked by mAb 41H16, heat-aggregated human IgG, or anti-MHC Class II mAb. Similarly, multimeric immune complexes composed to TT and anti-TT mAb, SA13, and 9F12 also enhanced presentation of TT. Furthermore, Fc gamma RII on purified human peripheral blood B cells could also enhance Ag presentation. These studies provide the first clear evidence that Fc gamma RII can participate in enhanced Ag presentation by human B cells and suggest that Fc gamma RII has the potential to play a stimulatory role in human B cell responses to Ag-Ab complexes.
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