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* Department of Immunology, St. Jude Children’s Research Hospital, Memphis, TN 38105; and
Trudeau Institute, Saranac Lake, NY 12983
Lymphocyte activation gene-3 (LAG-3) is a CD4-related, activation-induced cell surface molecule that binds to MHC class II with high affinity. In this study, we used four experimental systems to reevaluate previous suggestions that LAG-3–/– mice had no T cell defect. First, LAG-3–/– T cells exhibited a delay in cell cycle arrest following in vivo stimulation with the superantigen staphylococcal enterotoxin B resulting in increased T cell expansion and splenomegaly. Second, increased T cell expansion was also observed in adoptive recipients of LAG-3–/– OT-II TCR transgenic T cells following in vivo Ag stimulation. Third, infection of LAG-3–/– mice with Sendai virus resulted in increased numbers of memory CD4+ and CD8+ T cells. Fourth, CD4+ T cells exhibited a delayed expansion in LAG-3–/– mice infected with murine gammaherpesvirus. In summary, these data suggest that LAG-3 negatively regulates T cell expansion and controls the size of the memory T cell pool.
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