Patients infected with human immunodeficiency virus type 1 (HIV-1) often have dysfunctional dendritic cells (DCs), but as HIV-1 cannot directly infect these cells, the basis of this effect has been unclear. In the Journal of Clinical Investigation, Bhardwaj and colleagues show that apoptotic microparticles generated from lymphocytes mainly during acute HIV infection are responsible for this DC dysfunction. Serum, but not virus, isolated from HIV+ patients suppresses the Toll-like receptor (TLR)-mediated release of inflammatory cytokines by DCs. This effect on DCs seems to be HIV specific, because serum from patients acutely infected with hepatitis virus C or B is not inhibitory. Furthermore, microparticles in serum from uninfected patients are also unable to modulate DC function, which suggests that microparticles associated with HIV infection are somehow qualitatively distinct. Although the identity of the microparticle protein(s) remains unclear, CD44 expression by DCs is critical for its recognition and for mediation of the modulatory signal.
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Fehervari, Z. DC defects in HIV-1. Nat Immunol 14, 118 (2013). https://doi.org/10.1038/ni.2528
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DOI: https://doi.org/10.1038/ni.2528
