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Abstract
Previous studies have demonstrated the involvement of complement (C) in induction of efficient CTL responses against different viral infections, but the exact role of complement in this process has not been determined. We now show that C opsonization of retroviral particles enhances the ability of dendritic cells (DCs) to induce CTL responses both in vitro and in vivo. DCs exposed to C-opsonized HIV in vitro were able to stimulate CTLs to elicit antiviral activity significantly better than non-opsonized HIV. Furthermore, experiments using the Friend virus (FV) mouse model illustrated that the enhancing role of complement on DC-mediated CTL induction also occurred in vivo. Our results indicate that complement serves as natural adjuvant for DC-induced expansion and differentiation of specific CTLs against retroviruses.
Highlights
During the acute phase of HIV-1 infection the immune system responds with a massive, oligoclonal expansion of CD8+ T cells [1]
Since it is extremely difficult to investigate the role of HIV-complement interactions on the induction of virus-specific cytotoxic T lymphocytes (CTLs) in vivo, we used the well-characterized Friend virus (FV) mouse model for our in vivo studies
We show that complement opsonization of retroviral particles enhanced the ability of dendritic cells (DCs) to induce CTL responses against HIV or FV
Summary
During the acute phase of HIV-1 infection the immune system responds with a massive, oligoclonal expansion of CD8+ T cells [1]. A gradual failure of the immune response occurs due to a dramatic loss of CD4+ T cells, spontaneous apoptosis of non-infected, activated CD4+ and CD8+ T cells, induction of Tregs, escape of virus-specific CD8+ T cell recognition by HIV, and destruction of the follicular dendritic cell network [5]. In long-term non-progressors HIV-specific CTLs are suggested to be important mediators of protection due to increased anti-HIV CTL precursor numbers and lower viral burden [6]. Increasing evidence suggests an important role for the complement system in protection against viral infections. C activation contributes directly to host protection against viruses by C-mediated lysis or opsonization, but is essential in priming humoral responses as demonstrated for different viral infections [7,8,9]. Upon infection of C3-deficient mice with influenza virus, a significant impairment in priming of CD4+
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