test_moissonnage_selune
type: Agent

gp160 of HIV or anti-CD4 monoclonal antibody ligation of CD4 induces inhibition of JNK and ERK-2 activities in human peripheral CD4+ T lymphocytes.
type: Distribution
access URL: https://inserm.hal.science/inserm-00076828
format: HTML
issued: 2026-05-29T17:12:51.965889
modified: 2026-05-29T17:12:51.773380

gp160 of HIV or anti-CD4 monoclonal antibody ligation of CD4 induces inhibition of JNK and ERK-2 activities in human peripheral CD4+ T lymphocytes.
type: Dataset
contact point: Organization
  fn: CCSD
keyword: mesh-enzyme-activation
keyword: mesh-ca2-calmodulin-dependent-protein-kinase
keyword: mesh-humans
keyword: mesh-jnk-mitogen-activated-protein-kinases
keyword: infoeu-reposemanticsarticle
keyword: mesh-antigens-cd4
keyword: mesh-map-kinase-ki
keyword: mesh-antibodies-monoclonal
keyword: mesh-hiv-envelope-protein-gp160
keyword: sdvcanlife-sciences-q-biocancer
keyword: mesh-cd8-positive-t-lymphocytes
keyword: journal-articles
keyword: mesh-ligands
keyword: mesh-cd4-positive-t-lymphocytes
landing page: 0014-2980
description: Under physiological conditions, activation of CD4+ T cells by major histocompatibility complex (MHC)antigen complexes requires engagement of both the T cell receptor and the CD4 molecule. However, CD4 ligands binding to the CD4 molecule has also been shown to inhibit T cell proliferation and interleukin (IL)-2 production in human CD4+ T cells, in an MHC-independent way. We have previously shown that this inhibition was associated with a diminished binding activity of the IL-2 transcription factors NF-AT, NF-kappaB, and AP-1. AP-1 plays a key role in the regulation of IL-2 transcription, and ERK and JNK activities are necessary for regulating AP-1 at both the transcriptional and the post-transcriptional levels. We therefore studied, in human peripheral CD4+ T cells, the regulation of the activities of extracellular signal-regulated protein kinases (ERK) and c-Jun N-terminal kinases (JNK) by two CD4 ligands, gp160 the envelope glycoprotein of human immunodeficiency virus (HIV) and an anti-CD4 monoclonal antibody (mAb). Pre-incubation of CD4+ T lymphocytes in the presence of anti-CD4 mAb or gp160 inhibits the activation of JNK in response to phorbol 12-myristate 13-acetate and ionomycin. In the same conditions, phosphorylation and activation of ERK-2 were also inhibited. Inhibition of both JNK and ERK-2 activities are specific for binding of CD4 ligands to the CD4 molecule. They were not observed in CD8+ T lymphocytes. These results suggest that a specific inhibition of JNK and ERK-2 activities contributes to defective IL-2 production in T lymphocytes pre-incubated with CD4 ligands.
issued: 2026-05-29T17:12:51.821640
language: en
modified: 2026-05-29T17:12:51.821648