Document Detail


Diverse mechanisms and consequences of immunoadoption of neuromediator systems.
MedLine Citation:
PMID:  19076364     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Modern investigations of the mechanisms of both neuroregulation of immunity and neural effects of immune reactions have focused on identification of the mediators, their receptors, and signal transduction pathways in both systems. Less attention has been directed to delineation of the tissue context of neuroregulation of immunity that determines the principal sources of neuromediators, the physiological consequences of integration of neural and immune activities, and possible approaches to pharmacological manipulation. To illustrate these points, we describe here the corticotropin-releasing hormone (CRH) and vasoactive intestinal peptide (VIP) axes. When generated by the hypothalamus in response to inflammation or other stresses, CRH is immunosuppressive through its ability to increase levels of glucocorticoids and catecholamines. In contrast, CRH from peripheral nerves and immune accessory cells is immunostimulatory in tissue immune responses through direct effects on macrophages and lymphocytes. VIP released from several sets of nerves is immunosuppressive as a result of actions on macrophages and T cells in lymphoid organs, whereas VIP from immune cells in local tissue responses to antigen enhances development of some types of memory T cells and effector Th17 cells. Better understanding of how tissue context establishes the nature of neuroregulation of immunity will improve neuropharmacological and other neurotherapeutic approaches to immune diseases.
Authors:
Edward J Goetzl; Robert C Chan; Mahesh Yadav
Related Documents :
22272214 - Cucurbitacin e induces g(2)/m phase arrest through stat3/p53/p21 signaling and provokes...
21961024 - Involvement of prohibitin upregulation in abrin-triggered apoptosis.
22110774 - Isotretinoin and foxo1: a scientific hypothesis.
21738214 - Bid regulates aif-mediated caspase-independent necroptosis by promoting bax activation.
19027004 - Role of nuclear transcription factor kappa b (nf-kappab) for mptp (1-methyl-4-phenyl-1,...
8610904 - Lipoteichoic acid from staphylococcus aureus depresses contractile function of human ar...
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review    
Journal Detail:
Title:  Annals of the New York Academy of Sciences     Volume:  1144     ISSN:  1749-6632     ISO Abbreviation:  Ann. N. Y. Acad. Sci.     Publication Date:  2008 Nov 
Date Detail:
Created Date:  2008-12-16     Completed Date:  2009-02-19     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7506858     Medline TA:  Ann N Y Acad Sci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  56-60     Citation Subset:  IM    
Affiliation:
Department of Medicine and Microbiology-Immunology, University of California, San Francisco, CA 94143-0711, USA. edward.goetzl@ucsf.edu
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Corticotropin-Releasing Hormone / metabolism*
Humans
Models, Biological
Neuroimmunomodulation*
T-Lymphocytes / immunology,  metabolism
Vasoactive Intestinal Peptide / metabolism*
Grant Support
ID/Acronym/Agency:
AI 29912/AI/NIAID NIH HHS
Chemical
Reg. No./Substance:
37221-79-7/Vasoactive Intestinal Peptide; 9015-71-8/Corticotropin-Releasing Hormone

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  The Sall2 transcription factor is a novel p75NTR binding protein that promotes the development and f...
Next Document:  Substance P in stress and anxiety: NK-1 receptor antagonism interacts with key brain areas of the st...