Evidence map›Paper›PMID 19818725›Full record

ReviewBrain, behavior, and immunity2010

Depression and immunity: a role for T cells?

Andrew H Miller

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Brain, behavior, and immunity, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 163 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
163citing papers in PubMed, 3 pooled it
5.4field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

163 citing papers in PubMed, 3 syntheses or guidelines pooled it, 336 citations in OpenAlex.

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103 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Andrew H MillerEmory University School of Medicine, Atlanta, GA 30322, USA. amill02@emory.edu
Emory University · US

Funding

Phenotyping Major Depression with Increased InflammationR01MH087604 · NIMH · EMORY UNIVERSITY · PI MILLER, ANDREW H · 2010 to 2014
$2.2M
Dopaminergic Mechanisms of Cytokine-Induced Behavioral ChangeR01MH083746 · NIMH · EMORY UNIVERSITY · PI MILLER, ANDREW H · 2009 to 2012
$1.5M
Neuroimmune Mechanisms of Glucocorticoid ResistanceR01MH075102 · NIMH · EMORY UNIVERSITY · PI MILLER, ANDREW H · 2006 to 2010
$1.0M
Pathology and Treatment of Cytokine-Induced DepressionK05MH069124 · NIMH · EMORY UNIVERSITY · PI MILLER, ANDREW H · 2004 to 2008
$585k
NIMH NIH HHS K05 MH069124NIMH NIH HHS R01 MH075102NIMH NIH HHS R01 MH083746NIMH NIH HHS R01 MH087604
6 · The paper itself

Abstract

Much attention has been paid to the potential role of the immune system in the pathophysiology of major depression in humans. While activation of innate immune responses currently dominates the research landscape, early studies in depressed patients demonstrating impairment in acquired immune responses, in particular T cell responses, may warrant further consideration. Intriguing data suggest that activated T cells may play an important neuroprotective role in the context of both stress and inflammation. For example, generation of autoreactive T cells through immunization with central nervous system (CNS) specific antigens has been shown to reverse stress-induced decreases in hippocampal neurogenesis as well as depressive-like behavior in rodents. In addition, trafficking of T cells to the brain following stress, in part related to glucocorticoids, has been found to reduce stress-induced anxiety-like behavior. Data indicate that T regulatory cells may also play a role in depression through downregulation of chronic inflammatory responses. Based on the notion that T cells may subserve neuroprotective and anti-inflammatory functions during stress and inflammation, impaired T cell function may directly contribute to the development of depression. Indeed, increased sensitivity to apoptosis as well as reduced responsiveness to glucocorticoids, may not only decrease the availability of T cells in depressed patients, but also may reduce their capacity to traffic to the brain in response to relevant neuroendocrine or immune stimuli. Further elucidation of T cell pathology may lead to new insights into immune system contributions to depression. Moreover, enhancement of T cell function may represent an alternative strategy to treat depression.

Indexed as

AnimalsDepressive DisorderHumansImmunity, CellularInflammationT-Lymphocytes

Identifiers

PMID19818725
PMCPMC2787959
OpenAlexW2037084854

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.