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B, NF-AT, and Early Growth Factors 2/31
*
Department of Biological Sciences, Rutgers University, Newark, NJ 07102; and
Departamento Biologia Celular, Facultad de Biologia, Universidad Complutense, Madrid, Spain
Activation-induced cell death in T cells, a major mechanism
for limiting an ongoing immune response, is initiated by Ag
reengagement and mediated through Fas/Fas ligand interactions.
Vasoactive intestinal peptide (VIP) and pituitary adenylate
cyclase-activating polypeptide (PACAP), two multifunctional
neuropeptides, modulate innate and adaptive immunity. We reported
previously that VIP/PACAP protect T cells from activation-induced cell
death through down-regulation of Fas ligand (FasL). In this study, we
investigate the molecular mechanisms involved in the protective effect
of VIP and PACAP. VIP/PACAP reduce in a dose-dependent manner
anti-CD3-induced apoptosis in 2B4.11 T cell hybridomas. The
protective effect is mediated through the specific type 2 VIP receptor,
and the cAMP/protein kinase A pathway. A functional study demonstrates
that VIP/PACAP inhibit activation-induced FasL expression. VIP/PACAP
inhibit the expression and/or DNA-binding activity of several
transcriptional factors involved in FasL expression, i.e.,
c-myc, NF-
B, NF-ATp, and early growth factors (Egr)
2/3. The inhibition of NF-B binding is due to the stabilization of
I-B (inhibitory protein that dissociates from NF-B), through the
inhibition of I-B kinase 
activity. Subsequently, p65 nuclear
translocation is significantly reduced. The inhibition in NF-ATp
binding results from a calcineurin-independent reduction in NF-ATp
nuclear translocation. VIP/PACAP inhibit the expression of Egr2 and 3,
but not of Egr1. The effects on the transcriptional factors are
mediated through type 2 VIP receptor with cAMP as secondary
messenger.
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