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Significance Zinc deficiency is known to trigger lymphopenia, but the mechanisms behind zinc-mediated lymphocyte maintenance have been unclear. We demonstrated that zinc uptake into cells through the zinc transporter ZIP10 is essential for cell survival in early B-cell development. The ablation of ZIP10 caused an increase in caspase activity accompanied by reduced intracellular zinc in the early B-cell developmental stages. The JAK-STAT pathways regulated ZIP10 expression, and ZIP10 expression was correlated with STAT activation in B-cell lymphoma samples. Our results establish a physiological role for ZIP10 in early B-cell survival.

Zinc transporter SLC39A10/ZIP10 facilitates antiapoptotic signaling during early B-cell development