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RESEARCH COMMUNICATION |
-interferon production by antigen-stimulated type 1 helper T cells
a Departments of Medicine and Microbiology-Immunology, University of California Medical Center, San Francisco, California 94143-0711, USA;
b Department of Medicine, Stanford University School of Medicine, Stanford, California 94305, USA; and
c Department of Immunology, The Scripps Research Institute, La Jolla, California 92037, USA
Vasoactive intestinal peptide (VIP) is a neuroendocrine mediator
in immune tissues that affects many T cell functions through two
homologous high-affinity G-protein-coupled receptors, termed VIPR1 and
VIPR2. Antigen-stimulated secretion of
-interferon (IFN-
) by
sperm whale myoglobin-specific Th1 cells of DBA/2 mouse
I-Ed-restricted clones, which express VIPR1 and VIPR2, was
enhanced by 10-10 M to 10-7 M VIP.
Enhancement of IFN-
secretion reached a mean maximum of fourfold for
VIP and threefold for a VIPR2-selective agonist, without any effect of
a VIPR1-selective agonist. Secretion of IFN-
by PMA and
ionomycin-stimulated clones of Th1 cells was not altered by VIP.
Antigen-stimulated secretion of IFN-
by T cell receptor-transgenic,
influenza hemagglutinin-specific, and cytokine-differentiated mouse
lymph node Th1 cells, which also express VIPR1 and VIPR2, was enhanced
by 10-10 M to 10-8 M VIP. Enhancement of
IFN-
secretion increased to a maximum of 14-fold for VIP, 14-fold
for the VIPR2-selective agonist, and 20-fold for the VIPR1-selective
agonist. In contrast to VIP suppression of interleukin production and
lack of effect on IFN-
production by T cells stimulated with
anti-CD3 antibody or a mitogenic lectin, generation of IFN-
by
antigen-stimulated T cells is enhanced significantly by physiological
concentrations of VIP.Jabrane-Ferrat, N., Bloom, D., Wu, A., Li, L.,
Lo, D., Sreedharan, S. P., Turck, C. W., Goetzl, E. J.
Enhancement by vasoactive intestinal peptide of
-interferon
production by antigen-stimulated type 1 helper T cells.
Key Words: neuropeptide receptors G-proteins cytokines lymphocytes
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