期刊
JOURNAL OF IMMUNOLOGY
卷 169, 期 10, 页码 5392-5395出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.169.10.5392
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资金
- NCI NIH HHS [CA 09346, CA 21765, R25 CA023944, CA 23944] Funding Source: Medline
- NIAID NIH HHS [AI 07372, AI 39480] Funding Source: Medline
Lymphocyte activation gene (LAG)-3 (CD223) is a CD4-related activation-induced cell surface molecule that binds to MHC class II molecules with high affinity and negatively regulates T cell expansion and homeostasis. In this study, we show that LAG-3 inhibits CD4-dependent, but not CD4-independent, T cell function via its cytoplasmic domain. Although high affinity interaction with MHC class II molecules is essential for LAG-3 function, tailless LAG-3 does not compete with CD4 for ligand binding. A single lysine residue (K468) within a conserved KIEELE motif is essential for interaction with downstream signaling molecules. These data provide insight into the mechanism of action of this important T cell regulatory molecule.
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