Regulation of T cell receptor signaling by activation-induced zinc influx.
J Exp Med
; 208(4): 775-85, 2011 Apr 11.
Article
em En
| MEDLINE
| ID: mdl-21422171
ABSTRACT
Zinc is a trace element that is essential for innate and adaptive immune responses. In addition to being a structural element of many proteins, zinc also functions as a neurotransmitter and an intracellular messenger. Temporal or spatial changes in bioavailable zinc may influence the activity of several enzymes, including kinases and phosphatases. We provide evidence that zinc functions as an ionic signaling molecule after T cell activation. Cytoplasmic zinc concentrations increased within 1 min after T cell receptor (TCR) triggering, in particular in the subsynaptic compartment. The increase depended on the extracellular zinc concentrations and was inhibited by silencing zinc transporter Zip6. Increased zinc influx reduced the recruitment of SHP-1 to the TCR activation complex, augmented ZAP70 phosphorylation and sustained calcium influx. By calibrating TCR activation thresholds, increased extracellular zinc bioavailability facilitated the induction of T cell proliferative responses to suboptimal stimuli.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Zinco
/
Ativação Linfocitária
/
Receptores de Antígenos de Linfócitos T
/
Transdução de Sinais
Limite:
Adult
/
Humans
Idioma:
En
Revista:
J Exp Med
Ano de publicação:
2011
Tipo de documento:
Article