Abstract

T-bet, a Th1-specific T-box transcription factor, regulates Th1 development by inducing endogenous Th1 cytokines and IFN-γ. This study was conducted to determine if T-bet knockout mice exhibit resistance to stress-induced development of depression-like behaviors. The T-bet knockout mice significantly reduced depressive-like behaviors provoked by repeated restraint stress in an elevated plus-maze test (EPM), tail suspension test (TST), and forced swim test (FST). Moreover, stress-induced elevations of the pro-inflammatory cytokines were attenuated in T-bet deficient group. These results suggest that T-bet directly mediated stress-induced depression. Therefore, understanding T-bet function during stress represents an additional treatment strategy for depression. © 2011 Elsevier B.V.

Author keywords

Behavior; Cytokine; Depression; Monoamine; T-bet

Indexed keywords

EMTREE drug terms: cytokine; transcription factor T bet

EMTREE medical terms: animal experiment; article; controlled study; depression; disease resistance; elevated plus maze test; experimental test; forced swimming test; gene silencing; immobilization stress; male; maze test; mouse; nonhuman; priority journal; protein function; stress; tail suspension test

MeSH: Animals; Anxiety; Cytokines; Depression; Hindlimb Suspension; Inflammation Mediators; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Random Allocation; Restraint, Physical; Stress, Physiological; T-Box Domain Proteins
Medline is the source for the MeSH terms of this document.

Chemicals and CAS Registry Numbers: Cytokines; Inflammation Mediators; T-Box Domain Proteins; T-box transcription factor TBX21