期刊
JOURNAL OF IMMUNOLOGY
卷 181, 期 10, 页码 6707-6710出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.181.10.6707
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资金
- Korean government (Ministry of Education, Science, and Technology) [R0A-2008-000-20113-0]
- National Research Foundation of Korea [과C6A2102, R0A-2008-000-20113-0] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Invariant NKT (iNKT) cells are a distinct subset of T lymphocytes that recognize glycolipid Ags. Upon TCR stimulation, iNKT cells promptly secrete a wide range of cytokines and therefore have been investigated as a target for immunotherapy. However, after primary activation, iNKT cells become hyporesponsive toward their ligand (anergy). The further mechanism behind iNKT cell anergy is poorly understood. We found that a low level of programmed death-1 (PD-1) was constitutively expressed on iNKT cells and that PD-1 expression was increased after stimulation and lasted at least 2 mo. Moreover, not only did blocking of the PD-1/PD ligand 1 (PD-L1) pathway prevent the induction of anergy in iNKT cells, but anergic NKT cells also recovered responsiveness and these rescued cells efficiently mediated antitumor immunity. Our findings suggest that the PD-1/PD-L1 interaction is essential for the induction and maintenance of iNKT cell anergy. The Journal of Immunology, 2008,181: 6707-6710.
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