کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
3355672 1591573 2012 5 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Soluble B7-H1: Differences in production between dendritic cells and T cells
موضوعات مرتبط
علوم زیستی و بیوفناوری ایمنی شناسی و میکروب شناسی ایمونولوژی
پیش نمایش صفحه اول مقاله
Soluble B7-H1: Differences in production between dendritic cells and T cells
چکیده انگلیسی

Tumor cells aberrantly express several T cell inhibitory molecules including members of the B7-H co-regulatory family. Presumably tumor-expressed B7-H1 and B7-H3 confer resistance to elimination by the immune system. In addition, elevated levels of soluble B7-H1 (sB7-H1) has been identified in the sera of cancer patients, including renal carcinoma patients and is associated with increased cancer related death. Here we report that sB7-H1 is produced and released by activated mature dendritic cells (mDC). Immature DC, macrophages, monocytes, or T cells are refractory to releasing sB7-H1. Exposure of CD4+ and CD8+ T cells to mDC-derived sB7-H1 molecules induced apoptosis. These data suggest that the immunobiology of B7-H1 is perhaps more complex than previously thought. sB7-H1 molecules may represent an unanticipated contributing factor to immune homeostasis. That both immune and tumor cells can be sources of sB7-H1 suggests that optimization of co-regulatory blockade immunotherapy for solid malignancies of necessity will require impact of targeting tumor and immune-derived B7-H1 molecules.


► Soluble B7-H1 (sB7-H1) is released by activated mature dendritic cells (mean sB7-H1 270 pg/day × mL × 106 cells).
► Activated T cells release trace amounts of sB7-H1 (mean sB7-H1 <14 pg/day × mL × 106 cells) under optimal activation conditions.
► Dendritic cell-derived sB7-H1 induces apoptosis in T cells.
► Immune cell-derived sB7-H1 may mediate yet to described immune regulatory effects.
► B7-H1 blockade therapy may be impacted by immune-derived sB7-H1.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Immunology Letters - Volume 142, Issues 1–2, 29 February 2012, Pages 78–82
نویسندگان
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