International Immunology, Vol 10, 869-876, Copyright © 1998 by Oxford University Press
A Pallier, S Jauliac, N Jabado, A Fischer and C Hivroz
CD4 ligand binding to the CD4 molecules has been shown to inhibit T cell
proliferation and IL-2 transcription and synthesis. We have recently shown
that this inhibition correlated with a CD4-mediated inhibition of the
kinase Erk-2 and c-Jun-N-terminal kinases (JNK) which play a key role in
IL-2 transcription. Moreover, we have previously reported that
antigen-independent adhesion of CD45RObright/CD4+ T cells to B cells is
negatively regulated by CD4 ligands, whereas that of CD45RAbright/CD4+
naive T cells is not. Other groups have described, in murine models, a
differential sensitivity of memory and naive T cells to CD4-mediated
inhibitory effects on T cell activation. The aim of the present report was
to study the sensitivity of the naive and memory CD4+ T cell populations to
the CD4-mediated inhibition of Erk-2 and JNK activation. Our data show that
preincubation with anti-CD4 mAb, of the CD45RAbright/CD4+ naive and the
CD45RObright/CD4+ memory human T cell populations, induces inhibition of
both Erk-2 phosphorylation and Erk-2 activation by phorbol ester or
anti-CD3 mAb. In contrast, CD3 mediated JNK activation was inhibited in the
memory but not in the naive CD4+ T cell population, whereas JNK activation
by phorbol ester or phorbol esters plus Ca2+ ionophore was inhibited by
anti-CD4 mAb in both T cell populations. These data further demonstrate a
differential sensitivity of naive and memory CD4+ T cell populations to the
CD4-mediated negative signaling.
ARTICLES
Differential CD4-dependent inhibition of JNK but not Erk-2 activities in human naive and memory CD4+ T cell populations
INSERM U429, Pavillon Kirmisson, Hopital Necker-Enfants-Malades, Paris, France.
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