Enhanced delayed-type hypersensitivity and diminished immediate-type hypersensitivity in mice lacking the inducible VPAC2 receptor for vasoactive intestinal peptide

Edward J. Goetzl, Julia K. Voice, Sanbing Shen, Glenn Dorsam, Yvonne Kong, Katrine M. West, Christine F. Morrison, Anthony J. Harmar

Research output: Contribution to a Journal (Peer & Non Peer)Articlepeer-review

130 Citations (Scopus)

Abstract

Vasoactive intestinal peptide (VIP) and its G protein-coupled receptors, VPAC1R and VPAC2R, are prominent in the immune system and regulate many aspects of T cell-dependent immunity. In mouse T cells, VPAC1R is expressed constitutively, whereas VPAC2R is induced by immune stimuli. VPAC2R-null (VPAC2R-/-) mice on a C57BL/6 background are shown here to have normal basic immune characteristics, including serum Ig concentrations, blood levels of all leukocytes, and spleen number of total T cells (CD3+) and T cells bearing CD4, CD8, and CD28. Hapten-evoked cutaneous delayed-type hypersensitivity (DTH) was significantly enhanced in VPAC2R-null mice compared with age- and sex-matched wild-type mice. In contrast, generation of IgE anti-hapten antibodies and active cutaneous anaphylaxis were ≥70% lower in VPAC2R-null mice than in wild-type controls. Cytokine production by splenic CD4+ T cells, stimulated with adherent anti-CD3 plus anti-CD28 antibodies, revealed higher levels of IL-2 (mean = 3-fold) and IFN-γ (mean = 3-fold), and lower levels of IL-4 (mean = one-fifth) in VPAC2R-null mice than wild-type controls. Loss of VIP-VPAC2R maintenance of the normal ratio of Th2/Th1 cytokines thus leads to a state of enhanced DTH and depressed immediate-type hypersensitivity, which may alter both host defense and susceptibility to immune-mediated diseases.

Original languageEnglish
Pages (from-to)13854-13859
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume98
Issue number24
DOIs
Publication statusPublished - 20 Nov 2001
Externally publishedYes

Keywords

  • Cytokine
  • IgE
  • Immunity
  • Neuropeptide
  • T cell

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