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CD8+ cytotoxic T-APC stimulate central memoiry CD8+ T cell responses via acquired peptide-MHC class I complexes and CD80 costimulation, and RL-2 secretion
被引:39
作者:
Xia, Dajing
Hao, Siguo
Xiang, Jim
机构:
[1] Univ Saskatchewan, Res Unit, Saskatchewan Canc Agcy, Coll Med,Dept Oncol, Saskatoon, SK, Canada
[2] Univ Saskatchewan, Res Unit, Saskatchewan Canc Agcy, Coll Med,Dept Dept Microbiol & Immunol, Saskatoon, SK, Canada
关键词:
ANTIGEN-PRESENTING CELLS;
DENDRITIC CELLS;
LYMPH-NODES;
MEMORY;
ACTIVATION;
DIFFERENTIATION;
MOLECULES;
VIVO;
RECEPTOR;
INDUCE;
D O I:
10.4049/jimmunol.177.5.2976
中图分类号:
R392 [医学免疫学];
Q939.91 [免疫学];
学科分类号:
100102 ;
摘要:
We previously showed that naive CD4(+) Th cells acquire peptide-MHC class I (pMHC 1) and costimulatory molecules from OVA-pulsed dendritic cells(DCOVA), and act as Th-APCs in stimulation of CD8(+)CTL responses. In this study, we further demonstrated that naive CD8(+) cytotoxic T (Tc) cells also acquire pMHC I and costimulatory CD54 and CD80 molecules by DCOVA stimulation, and act as Tc-APC. These Tc-APC can play both negative and positive modulations in antitumor immune responses by eliminating DCOVA and neighboring Tc-APC, and stimulating OVA-specific CD8(+) central memory T responses and antitumor immunity. Interestingly, the stimulatory effect of Tc-APC is mediated via its IL-2 secretion and acquired CD80 co-stimulation, and is specifically targeted to OVA-specific CD8(+) T cells in vivo via its acquired pMHC I complexes. These principles could be applied to not only antitumor immunity, but also other immune disorders (e.g., autoimmunity).
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页码:2976 / 2984
页数:9
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