Regulation of T cell receptor signaling by activation-induced zinc influx.
J Exp Med
; 208(4): 775-85, 2011 Apr 11.
Article
de 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.
Texte intégral:
1
Collection:
01-internacional
Base de données:
MEDLINE
Sujet principal:
Zinc
/
Activation des lymphocytes
/
Récepteurs aux antigènes des cellules T
/
Transduction du signal
Limites:
Adult
/
Humans
Langue:
En
Journal:
J Exp Med
Année:
2011
Type de document:
Article
Pays d'affiliation:
États-Unis d'Amérique