EXPRESSION AND FUNCTION OF LOW-DENSITY-LIPOPROTEIN RECEPTORS IN CD3(-)CD16(- EFFECT OF INTERLEUKIN-2()CD56(+) CELLS )

Citation
Jb. Desanctis et al., EXPRESSION AND FUNCTION OF LOW-DENSITY-LIPOPROTEIN RECEPTORS IN CD3(-)CD16(- EFFECT OF INTERLEUKIN-2()CD56(+) CELLS ), Cellular immunology, 167(1), 1996, pp. 18-29
Citations number
44
Categorie Soggetti
Cell Biology",Immunology
Journal title
ISSN journal
00088749
Volume
167
Issue
1
Year of publication
1996
Pages
18 - 29
Database
ISI
SICI code
0008-8749(1996)167:1<18:EAFOLR>2.0.ZU;2-N
Abstract
Low-density Lipoprotein receptors (LDLR) have been shown to be express ed, internalized, and transcribed in CD3(-)CD16(+)CD56(+) cells. Only a low percentage (up to 12%) of NB cells express LDLR. Interleukin 2 ( IL-2) (1000 IU/ml) induced a threefold increase in the expression of L DLR on the cell surface that results from, at least in part, augmentat ion of LDLR turnover from the cytosol to the membrane. Scatchard analy sis revealed that IL-2 decreased the K-d of LDLR binding for LDL from 7.53 to 4.33 nM with an increment in the number of binding sites from 2500 up to 5000. Both the proliferative response and cytotoxic functio ns of these cells are affected by LDL. Low concentrations of LDL induc e an increase in the proliferative response (up to eightfold) and in t he cytotoxic response of NK: cells (up to fivefold). High concentratio n (more than 60 mu g/ml) of LDL hampers both proliferative response an d cytotoxic activity of NK cells. LDL did not affect the cytotoxic fun ctions of IL-2-activated NK cells. Overall, we have shown that LDLR is expressed on the surface of Nh cells and can be augmented by IL-2. Fu rthermore, we propose some insights into the mechanism responsible for the enhanced expression of LDLR on NR cell surface. in addition, our data clearly delineate that Il)LR plays an important role in the regul ation of proliferative responses and cytotoxic activity of these cells . (C) 1996 Academic Press,Inc.