Journal
JOURNAL OF IMMUNOLOGY
Volume 172, Issue 9, Pages 5450-5455Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.172.9.5450
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Funding
- NCI NIH HHS [CA-09346, CA-21765] Funding Source: Medline
- NHLBI NIH HHS [HL69502, HL63925] Funding Source: Medline
- NIAID NIH HHS [AI-42927, AI-39480, AI-07372] Funding Source: Medline
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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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