Molecular cloning of a C-type lectin superfamily protein differentially expressed by CD8 alpha(-) splenic dendritic cells
Details
Publication Year 2001-09,Volume 38,Issue #5,Page 365-373
Journal Title
MOLECULAR IMMUNOLOGY
Publication Type
Journal Article
Abstract
Dendritic cells (DC) are potent antigen presenting cells that activate naive T cells. It is becoming increasingly clear that DC are not a homogeneous cell population, but comprise different subpopulations that differ in ontogeny and function. To further the molecular characterisation of DC, we screened for genes that were differentially expressed amongst DC subsets and Could therefore give insight into their varying biological functions. Using Representational Difference Analysis (RDA) we identified a gene (CIRE) that is expressed at higher levels in the myeloid-related CD8 alpha (-) DC than in the lymphoid-related CD8 alpha (+) DC. CIRE is a 238 amino acid type II membrane protein, of approximately 33 kDa in size. whose extracellular region contains a C-type lectin domain. Northern blot analysis revealed that CIRE is almost exclusively expressed in DC and was not detected in organs Such as heart, brain, kidney, liver, and thymus. T cells failed to express message for CIRE, whilst B cells expressed very low levels. These data here further substantiated by Northern blot analysis of 18 cell lines of various origins (myeloid, macrophage, B and T cell) where only one cell line, which was of myeloid origin and Could give rise to DC, expressed mRNA for CIRE. Semi-quantitative RT-PCR suggested that CIRE is down-regulated upon activation. CIRE shares 57% identity with human DC-SIGN, a molecule that has been shown to be the li,-,and of ICAM-3 and that is also a receptor that binds HIV and facilitates trans-infection of T cells. (C) 2001 Elsevier Science Ltd. All rights reserved.
Publisher
PERGAMON-ELSEVIER SCIENCE LTD
Keywords
PRIMARY IMMUNE-RESPONSES; DC-SIGN; IN-VIVO; ENDOTHELIAL-CELLS; CD8 EXPRESSION; MOUSE THYMUS; T-CELLS; INFECTION; SEQUENCE; RECEPTOR
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Creation Date: 2001-09-01 12:00:00
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