apoptotic microparticles that are generated during HIV infection can bind to DCs via CD44 and inhibit the pro-inflammatory functions of these cells
Although the overall number of DCs in the blood is known to be decreased in patients infected with HIV, reports have been conflicting regarding whether the virus affects the pro-inflammatory functions of these cells. Frleta et al. therefore set out to determine whether factors in the serum of patients infected with HIV can affect DC function. They generated monocyte-derived DCs from healthy human donors and treated these cells with plasma from uninfected individuals or from individuals with acute HIV-1 infection. In response to Toll-like receptor (TLR) ligands, the two sets of DCs showed similar expression levels of MHC and co-stimulatory molecules. However, the production of pro-inflammatory cytokines was markedly inhibited in the DCs exposed to plasma from patients with HIV-1. In addition, DCs treated with such plasma were unable to prime T helper 1 (TH1) cell responses or promote the activation of natural killer cells. Plasma from patients with chronic HIV infection also inhibited DC functions, but not as potently as plasma from acutely infected patients. The authors found that the DC-inhibitory property first occurs in plasma during the stage of acute HIV infection when the number of viral copies in the blood increases. However, plasma isolated from patients with acute hepatitis B virus or acute hepatitis C virus infections did not inhibit TLR-mediated DC activation, even when plasma was isolated at a similar stage of viraemia.
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