CD80 expression is decreased in hyperplastic lymph nodes of HIV+ patients

Citation
C. Legendre et al., CD80 expression is decreased in hyperplastic lymph nodes of HIV+ patients, INT IMMUNOL, 10(12), 1998, pp. 1847-1851
Citations number
36
Categorie Soggetti
Immunology
Journal title
INTERNATIONAL IMMUNOLOGY
ISSN journal
09538178 → ACNP
Volume
10
Issue
12
Year of publication
1998
Pages
1847 - 1851
Database
ISI
SICI code
0953-8178(199812)10:12<1847:CEIDIH>2.0.ZU;2-D
Abstract
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.