| First Author | Voice J | Year | 2004 |
| Journal | J Immunol | Volume | 172 |
| Issue | 12 | Pages | 7289-96 |
| PubMed ID | 15187104 | Mgi Jnum | J:90832 |
| Mgi Id | MGI:3044848 | Doi | 10.4049/jimmunol.172.12.7289 |
| Citation | Voice J, et al. (2004) c-Maf and JunB mediation of Th2 differentiation induced by the type 2 G protein-coupled receptor (VPAC2) for vasoactive intestinal peptide. J Immunol 172(12):7289-96 |
| abstractText | Vasoactive intestinal peptide and its G protein-coupled receptors, VPAC(1) and VPAC(2), regulate critical aspects of innate and adaptive immunity. T cell VPAC(2)Rs mediate changes in cytokine generation, which potently increase the Th2/Th1 ratio and consequently shift the effector responses toward allergy and inflammation. To examine mechanisms of VPAC(2) promotion of the Th2 phenotype, we analyzed controls of IL-4 transcription in CD4 T cells from T cell-targeted VPAC(2) transgenic (Tg), VPAC(2) knockout, and wild-type (WT) mice. c-maf and junB mRNA, protein, and activity were significantly up-regulated to a higher level in TCR-stimulated CD4 T cells from Tg mice compared with those from knockout and WT C57BL/6 mice. In contrast, GATA3, T-bet, and NFATc levels were identical in WT and Tg CD4 T cells. Vasoactive intestinal peptide binding to VPAC(2) on CD4 T cells specifically induces an up-regulation of the Th2-type transcription factors c-Maf and JunB, which consequently enhances IL-4 and IL-5 production, leading to a Th2-type phenotype. |
