Abstract
The structurally related neuropeptides vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase activating polypeptide (PACAP) are released within the lymphoid organs following antigenic stimulation, and modulate the function of inflammatory cells through specific receptors. In activated macrophages, VIP and PACAP inhibit the expression at both mRNA and protein level of pro-inflammatory cytokines and chemokines, through effects on de novo expression or nuclear translocation of a number of transcription factors, i.e. NFkB, CREB, c-Jun, JunB, and IRF-1. In addition, VIP and PACAP promote Th2-type, and inhibit Th1-type responses in vivo and in vitro, through several mechanisms, including preferential survival of Th2 effectors and subsequent generation of Th2 memory cells. The function of VIP / PACAP as “macrophage deactivating factors” appears to be responsible for their protective effect in vivo in models of septic shock. Both deactivation of macrophages and inhibition of Th1-type responses appear to be responsible for the beneficial effect of VIP/PACAP in models of Th1-type autoimmune diseases such as rheumatoid arthritis.
Keywords: neuropeptides, vasoactive intestinal peptide, pituitary adenylate cyclase activating polypeptide, effector cells, macrophages
Current Pharmaceutical Design
Title: The Neuropeptides VIP / PACAP and T Cells: Inhibitors or Activators?
Volume: 9 Issue: 12
Author(s): Doina Ganea and Mario Delgado
Affiliation:
Keywords: neuropeptides, vasoactive intestinal peptide, pituitary adenylate cyclase activating polypeptide, effector cells, macrophages
Abstract: The structurally related neuropeptides vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase activating polypeptide (PACAP) are released within the lymphoid organs following antigenic stimulation, and modulate the function of inflammatory cells through specific receptors. In activated macrophages, VIP and PACAP inhibit the expression at both mRNA and protein level of pro-inflammatory cytokines and chemokines, through effects on de novo expression or nuclear translocation of a number of transcription factors, i.e. NFkB, CREB, c-Jun, JunB, and IRF-1. In addition, VIP and PACAP promote Th2-type, and inhibit Th1-type responses in vivo and in vitro, through several mechanisms, including preferential survival of Th2 effectors and subsequent generation of Th2 memory cells. The function of VIP / PACAP as “macrophage deactivating factors” appears to be responsible for their protective effect in vivo in models of septic shock. Both deactivation of macrophages and inhibition of Th1-type responses appear to be responsible for the beneficial effect of VIP/PACAP in models of Th1-type autoimmune diseases such as rheumatoid arthritis.
Export Options
About this article
Cite this article as:
Ganea Doina and Delgado Mario, The Neuropeptides VIP / PACAP and T Cells: Inhibitors or Activators?, Current Pharmaceutical Design 2003; 9 (12) . https://dx.doi.org/10.2174/1381612033455116
DOI https://dx.doi.org/10.2174/1381612033455116 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
- Author Guidelines
- Graphical Abstracts
- Fabricating and Stating False Information
- Research Misconduct
- Post Publication Discussions and Corrections
- Publishing Ethics and Rectitude
- Increase Visibility of Your Article
- Archiving Policies
- Peer Review Workflow
- Order Your Article Before Print
- Promote Your Article
- Manuscript Transfer Facility
- Editorial Policies
- Allegations from Whistleblowers
- Announcements
Related Articles
-
Tachykinins as Therapeutic Targets in Inflammation
Current Medicinal Chemistry - Anti-Inflammatory & Anti-Allergy Agents Exploring the Biological Potential of Urea Derivatives Against mPGES-1: A Combination of Quantum Mechanics, Pharmacophore Modelling and QSAR Analyses
Medicinal Chemistry Platelet Activation in Atherogenesis Associated with Low-Grade Inflammation
Inflammation & Allergy - Drug Targets (Discontinued) Recognition of the N-Terminal Histone H2A and H3 Peptides by Peptidylarginine Deiminase IV
Protein & Peptide Letters Role of Biomechanical Force in Stem Cell-Based Therapy for Cartilage Repair
Current Rheumatology Reviews Vascularization of Biomaterials for Bone Tissue Engineering: Current Approaches and Major Challenges
Current Angiogenesis (Discontinued) The Role of Tai Chi in Mental Health Management—Lessons Learned from Clinical Trials
Reviews on Recent Clinical Trials Metal Complexes, their Cellular Targets and Potential for Cancer Therapy
Current Pharmaceutical Design Drug Levels and Antibodies Against TNF-blockers in Spondyloarthritis and Rheumatoid Arthritis are Associated with the Activity but they do Not Predict it
Current Rheumatology Reviews Acid Sensing Ion Channels and Acid Nociception
Current Pharmaceutical Design New therapeutic effects of cilostazol in patients with ischemic disorders
Current Vascular Pharmacology New Tubulin Polymerization Inhibitor Derived from Thalidomide: Implications for Anti-Myeloma Therapy
Current Medicinal Chemistry Recent Advances on the Roles of NO in Cancer and Chronic Inflammatory Disorders
Current Medicinal Chemistry Development and Uses for Monoclonal Antibodies to Chemoattractant Receptors
Current Immunology Reviews (Discontinued) Analytical and Pharmacological Aspects of Therapeutic Drug Monitoring of mTOR Inhibitors
Current Drug Metabolism Diagnostics and Therapy of Antineutrophil Cytoplasmic Antibody (ANCA) Associated Vasculitides
Current Pharmaceutical Design Patents in Targets and Drugs for Unbalanced Cytokine and Chemokine Network Mediated Disorders
Recent Patents on Inflammation & Allergy Drug Discovery In Vivo Gamma Scintigraphic Evaluation and Determination of a Gastro-Resistant Etodolac Tablet in Humans
Combinatorial Chemistry & High Throughput Screening Chemokines and Chemokine Receptors Blockers as New Drugs for the Treatment of Chronic Obstructive Pulmonary Disease
Current Medicinal Chemistry Inhibitors of the Chemokine Receptor CXCR4: Chemotherapy of AIDS, Metastatic Cancer, Leukemia and Rheumatoid Arthritis
Letters in Drug Design & Discovery