HIV-1 GP120 BLOCKS JACALIN-INDUCED PROLIFERATIVE RESPONSE IN CD4(-CELLS - JACALIN AS A USEFUL SURROGATE MARKER FOR QUALITATIVE AND QUANTITATIVE DEFICIENCY OF CD4(+) T-CELLS IN HIV-1 INFECTION() T)

Citation
Sml. Tamma et al., HIV-1 GP120 BLOCKS JACALIN-INDUCED PROLIFERATIVE RESPONSE IN CD4(-CELLS - JACALIN AS A USEFUL SURROGATE MARKER FOR QUALITATIVE AND QUANTITATIVE DEFICIENCY OF CD4(+) T-CELLS IN HIV-1 INFECTION() T), Clinical immunology and immunopathology, 80(3), 1996, pp. 290-297
Citations number
27
Categorie Soggetti
Pathology,Immunology
ISSN journal
00901229
Volume
80
Issue
3
Year of publication
1996
Part
1
Pages
290 - 297
Database
ISI
SICI code
0090-1229(1996)80:3<290:HGBJPR>2.0.ZU;2-J
Abstract
Jacalin is a plant lectin that induces mitogenic responses selectively in CD4(+) T lymphocytes and has been shown to block infection by the human immunodeficiency virus type 1 (HIV-1) in a T lymphoid cell line, but the relationship of jacalin to the HIV envelope glycoprotein gp12 0 in its interaction with the CD4 molecule is unclear. Here we demonst rate that pretreatment of normal T cells with native HIV-1 gp120 impai rs their ability to proliferate and secrete IL-2 in response to jacali n. This effect was not observed with deglycosylated gp120, which fails to bind to CD4 molecule, or with gp120 that has been premixed with so luble CD4. Flow cytometric studies and Western blotting analysis indic ated that gp120 and jacalin compete with each other in binding to CD4 molecules. In HIV-infected patients, proliferative responses of PBMC i n response to jacalin were found to correlate quantitatively with perc entages of CD4(+) T cells but also showed a qualitative defect in comp arison to healthy volunteers based on responses that were correlated f or CD4(+) T cell numbers. These findings suggest that (i) gp120 and ja calin compete with each other for CD4 binding and (ii) jacalin might b e a useful surrogate marker for quantitative as well as qualitative de ficiency of CD4(+) T cells in HIV-1 infection. (C) 1996 Academic Press , Inc.