Delineation of a region of the human immunodeficiency virus type 1 gp120 glycoprotein critical for interaction with the CD4 receptor

Lasky, Laurence A.; Nakamura, Gerald; Smith, Douglas H.; Fennie, Christopher; Shimasaki, Craig; Patzer, Eric J.; Berman, Phillip W.; Gregory, Timothy J.; Capon, Daniel J.

doi:10.1016/0092-8674(87)90524-1

Cited by 820 publications

(493 citation statements)

References 43 publications

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“…6). It is noteworthy that neutralization by soluble CD4 of the DR12 peptide inhibitory effect was not equimolar, suggesting that not all peptides had the optimal conformation, as already observed in previous experiments [6], Finally, two gp 160-derived peptides ana logous to positions 418-434 and 449-464, respectively, known to participate to the binding of gpl60 to CD4 [18] were more potent in suppressing the adhesion of resting CD4+ Tcells than that of anti-CD3-or NKlL16-activated T cells ( Fig. 7; p <0.001 and p <0,0001, respectively, for concentrations of 0.4 pM and 4 jam).…”

Section: Inhibition Of Anti-cd3-and Nkil16-activated Cd4+supporting

confidence: 66%

“…The gpl60 is in contrast similarly able to inhibit adhesion of resting, anti-CD3-and NKIL16-pretreated Tcells, suggest ing that its effect either is more potent or relies on a different mechanism. The former hypothesis is more likely since the affinity of gpl60 for CD4 is much higher than that of MHC class II for CD4 [18].…”

Section: Discussionmentioning

confidence: 99%

“…However, putative CD4 ligands (gp 160-derived peptides that mimick the gpl60 binding site to CD4 [18] and the DR-12 peptide analogous to the 35-46 sequence of HLA class II (3, including the highly preserved RFDS sequence) that specifically inhibit adhesion of resting CD4+ Tcells to B cells were less active on T cells preactivated by CD3 cross-linking. These results, differing from those observed with resting CD4+ Tcells, may be explained by the higher affinity of LFA-l-mediated interactions [17].…”

Section: Discussionmentioning

confidence: 99%

“…Indeed, resting CD4+ T cells show similar maximal binding to MHC class II-positive and -negative B cells, although binding to class II+ B cells is transient whereas binding to class II" B cells is prolonged for at least 20 min. Finally, anti-CD4 antibodies and the gpl60 envelope protein from HIV (which binds to CD4; Coradoet al, submitted), as well as peptides encompassing the gp 160-binding site to CD4 [18] and peptides analogous to the 35-46 sequence of MHC class II (3 chains and containing the highly preserved RFDS sequence [19], all inhibit CD4'h T cell-B cell adhesion. This suggests that CD4-MHC class II interaction, possibly mediated in part by the MHC class II RFDS sequence, and gpl60 binding to CD4, can down-regulate antigen-independent adhesion of CD4+ Tcells.…”

Section: Introductionmentioning

confidence: 99%

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Regulation of LFA‐1‐mediated T cell adhesion by CD4

et al. 1991

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Heterotypic adhesion of T lymphocytes to monocytes, B lymphocytes, or other target cells is mainly mediated by LFA-1 and CD 2 molecules. Low-affinity binding of restingTcells can be transiently up-regulated by cross-linking of CD3. We have previously found that binding of specific ligands to CD4 can down-regulate adhesion of resting T cells to B cells. We now show that the enhanced adhesiveness of CD4+ T cells induced by CD3 cross-linking using plastic-bound anti-CD3 antibody can also be inhibited by several CD4 ligands, i.e. anti-CD4 antibodies, the gpl60 env protein of human immunodeficiency virus, as well as by putative CD4 ligands, i.e. synthetic peptides analogous to the gp 160-binding site to CD4 (positions 418-434 and 449-464) and a 12-mer synthetic peptide (DR-12) analogous to positions 35-46 of HLA class II |3 subunit and including the highly conserved Arg-Phe-Asp-Ser (RFDS) sequence» After CD3 cross-linking, maximal binding of Tcells to HLA class II-positive and -negative B cells was similar, although binding to HLA class II-negative B cells was more prolonged.Tcells that were passively induced to up-regulate adhesion by binding of a CD 1 la-specific antibody, NKIL16, known to enhance LFA-1-dependent adhesiveness, were less sensitive to the inhibitory effect of the DR-12 peptide, whereas the inhibitory effects of gpl60 were preserved. The kinetics of adhesion of NKIL16-pretreated T cells was not influenced by LILA class II expression at the B cell surface. Together, these results strongly suggest that CD4-HLA class II interaction may down-regulate low-affinity adhesion of resting T cells and, to some extent, high-affinity adhesion of T cells actively induced by CD3 cross-linking but not passively induced by an anti-CD 11a antibody 1 Introduction

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Section: Inhibition Of Anti-cd3-and Nkil16-activated Cd4+supporting

confidence: 66%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Regulation of LFA‐1‐mediated T cell adhesion by CD4

et al. 1991

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“…The only known molecular species expressed on the surface of D-54 cells capable of binding gp120 was found to be galactosyl-sulfatide. A similar molecule, GaiC, has been described to bind rgp120 with an affinity of 1.16 x 1 o-10 M (Harouse et al, 1991), which is higher than the affinity of rgp 1 20 binding to CD4 (2-5 x 1 o-s M; Lasky et al, 1987). We found that D-54 cells express two classes of binding sites with higher (1.2 x 1 o-10 M) and lower (3.2 x 1o-9 M) affinity to rgp120.…”

Section: Discussionmentioning

confidence: 99%

HIV-1 gp120 receptor on CD4-negative brain cells activates a tyrosine kinase

Schneider-Schaulies¹,

Schneider‐Schaulies²,

Brinkmann³

et al. 1992

Virology

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Human immunodeficiency virus (HIV-1) infection in the human brain Ieads to characteristic neuropathological changes, which may result indirectly from interactions of the envelope glycoprotein gp 120 with neurons and/or glial cells. We therefore investigated the binding of recombinant gp120 (rgp120) to human neural cells and its effect on int~acellular.s.ignallin~. Herewe pre~ent evidence that rgp120, besides binding to galactocerebroside or galactosyl-sulfatlde, spec1f1cally bmds to a protem receptor of a relative molecular mass of approximately 180,000 Da (180 kDa) pre~ent. on the CD4-negative glioma cells D-54, but not on Molt4 T lymphocytes. Binding of rgp120 to this receptor rap1dly 1nduced a tyrosine-specific protein kinase activity leading to tyrosine phosphorylation of 130-and 115-kDa p~oteins. The c~ncentration of intracellular calciumwas not affected by rgp120 in these cells. Our data suggest a novel Signal transduc1ng HIV-1 gp120 receptor on CD4-negative glial cells, which may contribute to the neuropathological changes observed in HIV-1-infected brains.

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Prospects for Prevention of and Early Intervention Against HIV

Bolognesi

1989

JAMA

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Delineation of a region of the human immunodeficiency virus type 1 gp120 glycoprotein critical for interaction with the CD4 receptor

Cited by 820 publications

References 43 publications

Regulation of LFA‐1‐mediated T cell adhesion by CD4

Regulation of LFA‐1‐mediated T cell adhesion by CD4

HIV-1 gp120 receptor on CD4-negative brain cells activates a tyrosine kinase

Prospects for Prevention of and Early Intervention Against HIV

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