CD1d on myeloid dendritic cells stimulates cytokine secretion from and cytolytic activity of Vα24JαQ T cells:: A feedback mechanism for immune regulation

被引:60
作者
Yang, OO
Racke, FK
Nguyen, PT
Gausling, R
Severino, ME
Horton, HF
Byrne, MC
Strominger, JL
Wilson, SB
机构
[1] Univ Calif Los Angeles, Div Infect Dis, Med Ctr, Los Angeles, CA 90095 USA
[2] Massachusetts Gen Hosp E, Ctr AIDS Res, Infect Dis Unit, Charlestown, MA 02129 USA
[3] Dana Farber Canc Inst, Boston, MA 02115 USA
[4] Genet Inst, Cambridge, MA 02140 USA
[5] Harvard Univ, Dept Mol & Cellular Biol, Cambridge, MA 02138 USA
[6] Johns Hopkins Univ, Dept Pathol, Baltimore, MD 21287 USA
关键词
D O I
10.4049/jimmunol.165.7.3756
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The precise immunologic functions of CD1d-restricted, CD161(+) AV24AJ18 (V alpha 24J alpha Q) T cells are not well defined, although production of IL-4 has been suggested as important for priming Th2 responses, However, activation of human V alpha 224J alpha Q T cell clones by anti-CD3 resulted in the secretion of multiple cytokines notably important for the recruitment and differentiation of myeloid dendritic cells. Specific activation of V alpha 24J alpha Q T cells was CD1d restricted. Expression of CD1d was found on monocyte-derived dendritic cells in vitro, and immunohistochemical staining directly revealed CD1d preferentially expressed on dendritic cells in the paracortical T cell zones of lymph nodes. Moreover, myeloid dendritic cells both activated V alpha 24J alpha Q T cells and were susceptible to lysis by these same regulatory T cells. Because myeloid dendritic cells are a major source of IL-12 and control Th1 cell differentiation, their elimination by lysis is a mechanism for limiting the generation of Th1 cells and thus regulating Th1/Th2 responses.
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收藏
页码:3756 / 3762
页数:7
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