Accumulation of DC-SIGN+CD40+ dendritic cells with reduced CD80 and CD86 expression in lymphoid tissue during acute HIV-1 infection

Abstract

In the early phase of HIV-1 infection, there was a migration of DC to LT comparable to that found in acute EBV infection. The infiltration of DC in LT in acute EBV infection was accompanied by upregulation of CD80 and CD86 expression, which did not occur in aHI. This co-stimulatory defect in aHI may have an impact on the development of HIV-1-specific T cell immunity.

Dynamic Populations of Dendritic Cell-Specific ICAM-3 Grabbing Nonintegrin-Positive Immature Dendritic Cells and Liver/Lymph Node-Specific ICAM-3 Grabbing Nonintegrin-Positive Endothelial Cells in the Outer Zones of the Paracortex of Human Lymph Nodes

“…A similar increase in the number of mature DC-SIGN ϩ DCs has been reported during acute Epstein-Barr virus infections. 34 However, no changes in DC-SIGN-and L-SIGN-expressing cells in the paracortical outer zone were observed as determined by double stainings (not shown), although the amount of L-SIGN ϩ sinus endothelial cells increased dramatically in enlarged lymph nodes (Figure 4C, right).…”

Local and Systemic Effects of Intranodally Injected CpG-C Immunostimulatory-Oligodeoxyribonucleotides in Macaques

“…Reduced numbers of circulating DCs have been reported in HIVinfected people, correlating with increased virus load (27)(28)(29)(30)(31), suggesting possible redistribution of DCs from the periphery to the lymphoid tissues. However, the number of interdigitating DCs is reduced in patients with AIDS (32). The expression of costimulatory molecules CD80 and CD86 on LN DCs during HIV infection might be insufficient for induction of adequate antiviral responses (32).…”

“…However, the number of interdigitating DCs is reduced in patients with AIDS (32). The expression of costimulatory molecules CD80 and CD86 on LN DCs during HIV infection might be insufficient for induction of adequate antiviral responses (32). Macaque studies also demonstrated that DC maturation and frequency in LNs are affected during SIV infection (33,34).…”

Mechanism of T cell exhaustion in a chronic environment

“…1). Indeed, it has been reported that some viral and bacterial proteins expressed inside cells directly interfere with T cell priming by modulating the expression of MHC or co-stimulatory molecules (57)(58)(59)(60). Consequently, dominant and subdominant epitopes are not efficiently presented to T cells, which means that T cells are not optimally activated or often tolerated in some cases.…”