Comment on “TCR Activation Eliminates Glutamate Receptor GluR3 from the Cell Surface of Normal Human T Cells, via an Autocrine/Paracrine Granzyme B-Mediated Proteolytic Cleavage”

B eing strongly interested in the role of glutamate in the immune system and more specifically on its effects on lymphocyte physiology, we read the paper by Ganor et al. (1) with great interest. We would like to complement the authors for the clear and, for the most part, very well documented data. However, a potentially critical question was raised that we would like to bring to the authors’ kind attention and ask for clarification. The question concerns the use of RPMI 1640 as a culture medium in experiments where the effects of 10 nM glutamate were studied. The authors test the ability of 10 nM glutamate to induce T cell adhesion to laminin while cells are bathed in RPMI 1640, a medium with a glutamate concentration of 100 M (20 mg/L). Could the authors explain how they voided glutamate from the medium and thus were able to evaluate the effects of such a low concentration of glutamate?