Document Detail


Depression is an inflammatory disease, but cell-mediated immune activation is the key component of depression.
MedLine Citation:
PMID:  20599581     Owner:  NLM     Status:  In-Data-Review    
Abstract/OtherAbstract:
The first findings that depression is characterized by cell-mediated immune activation and inflammation were published between 1990-1993 (Maes et al.). Recently, it was reported that - based on meta-analysis results - depression is an inflammatory disorder because the plasma levels of two cytokines are increased, i.e. interleukin-(IL)-6 and tumor necrosis factor-α (TNFα). The same meta-analysis found that plasma IL-2 and interferon-(IFN)γ levels are not altered in depression, suggesting that there is no T cell activation in that illness. The present paper reviews the body of evidence that depression is accompanied by cell-mediated immune activation. The findings include: increased serum levels of the soluble IL-2 receptor (sIL-2R) and the sCD8 molecule; increased numbers and percentages of T cells bearing T cell activation markers, such as CD2+CD25+, CD3+CD25+, and HLA-DR+; increased stimulated production of IFNγ; higher neopterin and sTNFR-1 or sTNFR-2 levels; induction of indoleamine 2,3-dioxygenase (IDO) with lowered levels of plasma tryptophan and increased levels of tryptophan catabolites along the IDO pathway (TRYCATs); and glucocorticoid resistance in immune cells. Interferon-α (IFNα)-based immunotherapy shows that baseline and IFNα-induced activation of T cells, IDO activity and TRYCAT formation are related to the development of IFNα-induced depressive symptoms. Animal models of depression show that a cell-mediated immune response is related to the development of depression-like behavior. Antidepressants and mood stabilizers suppress different aspects of cell-mediated immunity and rather specifically target IFNγ production. This review shows that inflammation and cell-mediated immune activation are key factors in depression.
Authors:
Michael Maes
Publication Detail:
Type:  Journal Article     Date:  2010-06-20
Journal Detail:
Title:  Progress in neuro-psychopharmacology & biological psychiatry     Volume:  35     ISSN:  1878-4216     ISO Abbreviation:  Prog. Neuropsychopharmacol. Biol. Psychiatry     Publication Date:  2011 Apr 
Date Detail:
Created Date:  2011-04-18     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8211617     Medline TA:  Prog Neuropsychopharmacol Biol Psychiatry     Country:  England    
Other Details:
Languages:  eng     Pagination:  664-75     Citation Subset:  IM    
Copyright Information:
Copyright © 2010 Elsevier Inc. All rights reserved.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:

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


Previous Document:  Regulated delayed expression of rfc enhances the immunogenicity and protective efficacy of a heterol...
Next Document:  Dynamic causal modelling of anticipatory skin conductance responses.