VIP/PACAP preferentially attract Th2 effectors through differential regulation of chemokine production by dendritic cells MARIO DELGADO * , ELENA GONZALEZ-REY * and DOINA GANEA † ,1 * Instituto de Parasitologica y Biomedicina, CSIC, Granada, Spain; and † Department of Biological Sciences, Rutgers University, Newark, New Jersey, USA 1 Correspondence: Rutgers University, Dept. Biological Sciences, 101 Warren St., Newark, NJ 07102, USA. E-mail: dganea@andromeda.rutgers.edu <h3>SPECIFIC AIMS</h3> Vasoactive intestinal peptide (VIP) and the structurally related pituitary adenylate cyclase-activating polypeptide (PACAP) act as potent anti-inflammatory agents. In addition to direct suppressive effects on activated macrophages/microglia, neuropeptides also promote Th2-type responses. VIP, produced and secreted by Th2 cells following antigen stimulation, participates in a Th2 autoregulatory loop. VIP/PACAP affects differentiation of CD4 + T cells directly and indirectly through antigen presenting cells, and promotes proliferation and/or survival of Th2 effectors. Th1 and Th2 effectors express different chemokine receptors that control migration in response to various chemokines. In this study we investigated effects of VIP/PACAP on the production of CXCL10 (a Th1 chemokine) and of CCL22 (a Th2 chemokine) by bone marrow-derived dendritic cells. We found that VIP and PACAP inhibit CXCL10, while promoting CCL22 production, and that the effects are mediated through
/lp/fed-of-american-socs-for-experimental-biology/vip-pacap-preferentially-attract-th2-effectors-through-differential-K88co7Efmq