A synthetic peptide with sequence identity to the transmembrane protein GP41 of HIV-1 inhibits distinct lymphocyte activation pathways dependent on protein kinase C and intracellular calcium influx

Détails

ID Serval
serval:BIB_073E6372A8F8
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
A synthetic peptide with sequence identity to the transmembrane protein GP41 of HIV-1 inhibits distinct lymphocyte activation pathways dependent on protein kinase C and intracellular calcium influx
Périodique
Cellular Immunology
Auteur(s)
Ruegg  C. L., Strand  M.
ISSN
0008-8749 (Print)
Statut éditorial
Publié
Date de publication
10/1991
Volume
137
Numéro
1
Pages
1-13
Notes
In Vitro
Journal Article
Research Support, U.S. Gov't, P.H.S. --- Old month value: Oct 1
Résumé
A synthetic peptide containing env amino acid (aa) sequence 581 to 597 of the transmembrane protein gp41 of human immunodeficiency virus type 1 (HIV-1) was tested for its effect on protein kinase C (PKC) and cytoplasmic free Ca2+ [( Ca2+]i) influx-dependent immune functions. We have previously shown that this peptide inhibits PKC-mediated phosphorylation and T-cell receptor-mediated [Ca2+]i influx as well as lymphoproliferation. In this study we demonstrate that the HIV-1 gp41 peptide aa581-597 inhibits lymphoproliferation stimulated via the distinct T-cell-activation molecules CD3, CD2, and CD28, as well as direct stimulation mediated by phorbol ester combined with ionomycin. Further, aa581-597 inhibits both PKC-dependent interleukin 2 (IL 2) production and the [Ca2+]i influx-dependent but PKC-independent induction of IL 2 receptor expression. The HIV-1 gp41 peptide also induces dramatic morphologic changes in lymphocytes, characterized by cytoplasmic ballooning and the acquisition of adherence to plastic, and these changes are dependent on both the length and the temperature of exposure. The results of this study suggest that the HIV-1 gp41 sequence aa581-597 acts at multiple sites to inhibit both PKC activity and [Ca2+]i influx, resulting in the abrogation of several distinct immune functions that are critical for an intact immune response and are defective in HIV-1-infected individuals.
Mots-clé
Antigens, CD/physiology Antigens, CD3 Antigens, Differentiation, T-Lymphocyte/physiology Calcium/*physiology Cell Line HIV Envelope Protein gp41/*chemistry/pharmacology HIV-1/*immunology Humans Immune Tolerance Interleukin-2/biosynthesis *Lymphocyte Activation Peptides/pharmacology Protein Kinase C/*physiology Receptors, Antigen, T-Cell/physiology Receptors, Interleukin-2/metabolism Signal Transduction T-Lymphocytes/*immunology
Pubmed
Web of science
Création de la notice
28/01/2008 9:36
Dernière modification de la notice
20/08/2019 13:29
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