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PHENOTYPIC AND FUNCTIONAL CELLULAR DIFFERENCES BETWEEN HUMAN CD3(-) DECIDUAL AND PERIPHERAL-BLOOD LEUKOCYTES

Date
1994
Author
CHRISTMAS, SE
JOHNSON, PM
BREW, R
DENİZ, Günnur
Metadata
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Abstract
CD3(-) leukocyte clones derived from human decidualized endometrial tissue of first trimester pregnancy have been compared with CD3(-) PBL clones. Most CD3(-) decidual granulated leukocyte (DGL) clones were CD16(-) CD56(+) whereas most CD3(-) PBL clones were CD16(+) CD56(+). CD3(-) DGL and PBL clones, whether CD16(+) or not, showed MHC-nonrestricted NK cell activity. However, CD3(-) CD16(-) DGL clones had low cytotoxic activity against the NK-resistant cell line BSM, whereas CD3(-) CD16(+) DGL and CD3(-) PBL clones were strongly cytotoxic. Cytolytic activity has also been investigated in respect of target cell HLA-G expression, because this nonpolymorphic class I MHC molecule is expressed selectively by invasive fetal cytotrophoblast. Class I HLA Ag loss cell mutants were killed efficiently by CD3(-) DGL clones. Expression of transfected HLA-B8 increased their sensitivity to lysis by most CD3(-) DGL clones, whereas expression of transfected HLA-G commonly led to decreased target cell killing. In addition, the effects of uncloned CD3(-) DCL on the one-way MLR have been examined. These cells were very poor responders and, unless cultured to induce expression of class II MHC molecules, were also very poor stimulators. When fresh CD3(-) DGLs were added as third-party cells, either autologous or allogeneic to responder cells, [H-3]TdR incorporation was decreased in the MLR. Thus, CD3(-) DGL clones express MHC-nonrestricted cytolytic activity, notably against HLA-negative cells, but expression of HLA-G offers protection to target cells. In addition, CD3(-) DGL may function to suppress allogeneic responses.
URI
http://hdl.handle.net/20.500.12627/178622
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Creative Commons Lisansı

İstanbul Üniversitesi Akademik Arşiv Sistemi (ilgili içerikte aksi belirtilmediği sürece) Creative Commons Alıntı-GayriTicari-Türetilemez 4.0 Uluslararası Lisansı ile lisanslanmıştır.

DSpace software copyright © 2002-2016  DuraSpace
Contact Us | Send Feedback
Theme by 
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