 | NEUROENDOCRINE AND NEURAL REGULATION OF AUTOIMMUNE AND INFLAMMATORY DISEASE: Molecular, Systems, and Clinical Insights
Copyright © 2003 by the New York Academy of Sciences
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Annals of the New York Academy of Sciences 992:141-157 (2003)
© 2003 New York Academy of Sciences
PACAP in Immunity and Inflammation
MARIO DELGADO,
CATALINA ABAD,
CARMEN MARTINEZ,
M. GUILLERMA JUARRANZ,
JAVIER LECETA,
DOINA GANEAa AND
ROSA P. GOMARIZ
Department of Cell Biology, School of Biology, Complutense University, Madrid 28040, Spain
aRutgers University, Department of Biological Sciences, Newark, New Jersey 07102, USA
Address for correspondence: M. Delgado, Instituto de Parasitologia y Biomedicina Lopez Neyra, CSIC, Granada 18001, Spain. Voice: 34-958-805056; fax: 34-958-203323.
mdelgado{at}ipb.csic.es
Ann. N.Y. Acad. Sci. 992: 141-157 (2003).
The pituitary adenylate cyclase-activating polypeptide (PACAP) is a neuropeptide belonging to the VIP/secretin/glucagon family of peptides, produced by the lymphoid cells, which exerts a wide spectrum of immunological functions controlling the homeostasis of immune system through different receptors expressed in various immunocompetent cells. In the last decade, PACAP has been clearly identified as a potent anti-inflammatory factor that exerts its function by regulating the production of both anti- and proinflammatory mediators. In this sense, PACAP prevents death by septic shock, an acute inflammatory disease with a high mortality. In addition, PACAP regulates the expression of costimulatory molecules, inasmuch as this related to the modulation in the shift from Th1 towards Th2 differentiation. We recently reported that PACAP prevents the deleterious effects of arthritis by downregulating both inflammatory and autoimmune components of the disease. Therefore, PACAP and analogs have been proposed as very promising candidates, alternative to other existing treatments, for treating acute and chronic inflammatory and autoimmune diseases, such as septic shock, arthritis, multiple sclerosis, Crohn's disease, or autoimmune diabetes.
Key Words: neuroimmunology • inflammation • autoimmune diseases • rheumatoid arthritis • activation-induced cell death • neuropeptides • endotoxic shock • cytokines • chemokines • endotoxin • apoptosis • costimulatory response • differentiation • Th1 and Th2 cells • anti-inflammatory agents • therapeutic application • TNF-  • transcription factors • macrophages • vasoactive intestinal peptide (VIP)
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