کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9230101 | 1203611 | 2005 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Characterization of CD200-Receptor Expression in the Murine Epidermis
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کلمات کلیدی
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
امراض پوستی
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چکیده انگلیسی
CD200 is a widely expressed transmembrane glycoprotein that transmits an inhibitory signal after ligation of the structurally homologous CD200-receptor-1 (CD200R1). Recently, we showed that CD200 is expressed on keratinocytes and plays a role in protecting hair follicles from autoimmune attack. Here, we report the characterization of cell surface and mRNA expression of CD200R1 by cells of the murine epidermis. In addition, we report mRNA expression for other members of the CD200R-family (R2-R4) by quantitative real-time RT-PCR. Variable levels of CD200R1, R2, R3, and R4 mRNA were detected in bulk epidermal cell suspensions. Freshly isolated Langerhans cells (LC) preferentially expressed CD200R1. Consistent with an inhibitory role for CD200:CD200R1 interaction, LC obtained from mice deficient in CD200 (CD200-/-) were in a heightened state of activation as compared with wild-type (CD200+/+) cells. Freshly isolated dendritic epidermal T cells (DETC) expressed low levels of CD200R1, R2, and R3 mRNA, but they preferentially increased cell surface and mRNA expression of CD200R1 upon activation in vitro. In functional assays using sub-optimal CD3 signaling, immobilized CD200 inhibited DETC proliferation and cytokine secretion. Collectively, these results suggest that CD200:CD200R interactions may play a role in regulating both LC and DETC in cutaneous immune reactions.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Investigative Dermatology - Volume 125, Issue 6, December 2005, Pages 1130-1138
Journal: Journal of Investigative Dermatology - Volume 125, Issue 6, December 2005, Pages 1130-1138
نویسندگان
Michael D. Rosenblum, Jeffrey E. Woodliff, Nathaniel A. Madsen, Laura J. McOlash, Melissa R. Keller, Robert L. Truitt,