Biology Reference
In-Depth Information
F i g u r e 5.5. CD80 expression on CD19
B cells. Cell suspensions from one tonsil and one HIV
patient were labeled with phycoerythrin (PE)-CD80 and ¯uorescein isothiocyanate (FITC)-CD19
mAbs (A and C ) or with FITC-CD86 and PE-CD19 mAbs (B and D). Analysis was performed on
10,000 viable cells. Unshaded and shaded histograms are the control and CD80 or CD86 labeling,
respectively.
sion (Boussiotis et al., 1996; Somoza and Lanier, 1995). Thus, the low level of
CD80 in HIV
patients might result from inadequate T/B or FDC/B inter-
actions and/or being associated with GC depolarization. Soluble factors re-
leased by T cells or HIV-presenting FDC may also a¨ect CD80 expression on B
cells ( Reiser and Stadecker, 1996; Somoza and Lanier, 1995). The loss of CD80
may lead to more CD86/CD28 interactions, increasing HIV-1 replication
within the GC (Krzysiek et al., 1998), and leading to a shift toward T-helper 2
( TH2) T-cell responses, as previously reported ( Klein et al., 1997). It has been
suggested that preferential interactions occur between CD80 and CTLA-4
antigens ( Boussiotis et al., 1996). CTLA-4 may exert feedback control on the
T-cell response ( Tivol et al., 1995), so the loss of CD80 may be involved in
maintaining hyperplasia. Thus, hyperplasia a¨ects both centroblast and cen-
