A centrofollicular hyperplasia is present within secondary lymphoid organs
during all the asymptomatic phase of the HIV disease, Although this hyperpl
asia has been well characterized by histological studies, the nature of the
phenotypic alterations in B cell populations occurring within HIV+ lymphoi
d organs remains to be established. By immunohistochemistry, we thus invest
igated whether a particular germinal center (GC) B cell population was incr
eased during HIV-induced hyperplasia and whether any phenotypic change was
specific to HIV-1 infection, As compared to normal tonsils (three cases) an
d HIV- hyperplastic lymph nodes (eight patients), we observed a loss of GC
polarization in all HIV+ sections (11 patients), with no more delineation b
etween dark and light zones, as shown by Ki67, CD10, CD77, CD95 and CD86 st
aining. In contrast to CD86 expression which remained as intensive in HIVas in HIV- lymph nodes, CD80 staining was strongly decreased in GC of HIVlymph nodes but not in their extrafollicular zones. The loss of CD80 expres
sion from CD19(+) B cells was also observed by cytometric analysis of cell
suspensions of three HIV+ patients. Although we found no evidence of an inc
rease in a particular GC B cell subset in HIV-1-induced hyperplasia, the st
rong GC disorganization observed may induce impaired cell-cell interactions
and thus participate in the loss of CD80 antigen. In contrast to HIV- situ
ations where CD80 and CD86 was similarly expressed on B cells, the lower le
vel of CD80 expression in HIV+ GC may favor T(h)2 T cell responses through
CD86-CD28 interactions.