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* Departments of Medicine and Microbiology-Immunology, University of California Medical Center, San Francisco, CA 94143; and
Departments of Pathology and Laboratory Medicine, University of Texas Health Science, Houston, TX 77030
Vasoactive intestinal peptide (VIP) and its two G protein-coupled
receptors, VPAC1 and VPAC2, are quantitatively
prominent and functionally critical in the immune system. Transgenic
(T) mice constitutively expressing VPAC2 selectively in CD4
T cells, at levels higher than those found after maximal induction in
CD4 T cells of wild-type (N) mice, have elevated blood concentrations
of IgE, IgG1, and eosinophils; enhanced immediate-type
hypersensitivity; and reduced delayed-type hypersensitivity. In
contrast, VPAC2-null (K) mice manifest decreased
immediate-type hypersensitivity and enhanced delayed-type
hypersensitivity. The phenotypes are attributable to opposite skewing
of the Th2/Th1 cytokine ratio, but no studies were conducted on the
roles of T cell-derived VIP and altered expansion of the Th subsets.
Dependence of the Th phenotype of T mice, but not of N or K mice, on T
cell-derived VIP now is proven by showing that eliminating VIP from
TCR-stimulated T cell cultures with VIPase IgG normalizes the elevated
number of IL-4-secreting CD4 T cells, decreases the secretion of IL-4
and IL-10, and increases the secretion of IFN-
. Flexible
responsiveness of CD4 T cells from N and K mice, but not T mice, to
exogenous VIP in vitro and in vivo is shown by increased numbers of
IL-4-secreting CD4 T cells, greater secretion of IL-4 and IL-10, and
lesser secretion of IFN- after TCR stimulation with VIP. The level
of VIP recognized by CD4 T cells thus is a major determinant of the
relative contributions of Th subsets to the immune effector
phenotype.
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