Background:  Dendritic cells (DC) are the most potent antigen-presenting cells and play an important role in HIV pathogenesis. Myeloid DC play an important role in antigen uptake and T cell activation, whereas the plasmacytoid DC secret interferon (IFN) -a providing antiviral innate immunity. Impaired antigen presentation by dendritic cells during HIV infection could be caused either by the depletion of DC or by the reduced expression of co-stimulatory molecules (CD80 and CD86) important for antigen presentation. Myeloid and plasmacytoid DC populations and surface expression of co-stimulatory molecules; CD80 and CD86, were estimated in HIV⁺ individuals to study role of DC in HIV infection.

Methods:  The study participants were ART-naïve HIV-seropositive individuals comprising 8 recent seroconvertors, 13 AIDS patients (CD4<200 cells/mm³), and 9 slow progressors (asymptomatic with CD4 counts>500 cells/mm³ for longer than 3 years). Included as controls were 12 healthy HIV-seronegative individuals. DC were identified as the lineage-negative (CD3, CD14, CD16, CD19, CD20, and CD56), HLA-DR⁺ population and the 2 subpopulations were further differentiated by CD11c expression using flow cytometry. The surface expression of CD80 and CD86 was quantified as mean fluorescence intensity (MFI).

Results:  The number of myeloid DC was significantly lower in AIDS patients (p <0.01), whereas the number of plasmacytoid DC was significantly lower in the recently seroconverted (p <0.05) and AIDS patients (p <0.01) as compared to the control group. The AIDS patients showed significantly increased expression of CD80 in myeloid DC and CD86 in both myeloid and plasmacytoid DC (p <0.01 in all cases) as compared to the control group.

Conclusions:  The reduction in the number of plasmacytoid DC in HIV-infected individuals might be responsible for the impairment of immune response against the virus. The increased expression of co-stimulatory molecules in patients with advanced disease might be a result of activation of the DC by the increased viral multiplication. Both early HIV infection and slow progression was associated with increased number of blood DC and lower expression of co-stimulatory molecules compared to AIDS patients indicating that DC may have important role to play in disease progression. It will also be relevant to look at the same parameters in the mucosal DC, as well as DC in lymph nodes to understand the mechanisms of immune pathogenesis in chronic and advanced HIV infection.