In sharp contrast, however, although Selplg-/-memory T cells responded effectively to restimulation by LCMV viral peptides in vitro and did not exhibit greater susceptibility to death in the context of TCR engagement in vivo, they failed to respond to a secondary challenge with LCMV Arm after adoptive transfer with WT cells into the same naïve host, thus suggesting that inhibition via PSGL-1 during memory T cell activation may limit excessive stimulation induced by viral infection. This evidence concerns the gene SELPLG and viral infectious disease.