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No evidence for apoptosis of decidual leucocytes in normal and molar pregnancy: Implications for immune privilege

Lookup NU author(s): Dr Judith Bulmer, Dr Roger Searle

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Abstract

Complete hydatidiform moles are totally paternally derived and represent complete allografts that might be expected to provoke maternal immune rejection. Our previous and other studies have shown expression of Fas by increased numbers of activated decidual CD4+ T cells in both complete and partial molar pregnancy as well as increased FasL+ expression by molar trophoblasts compared with trophoblasts in normal pregnancies. As the Fas/FasL system represents a major apoptotic pathway that can play a role in immune privilege, the aim of this study was to investigate whether apoptosis of decidual immune cells, particularly T cells, could be responsible for maternal immune tolerance in molar pregnancy. Using terminal deoxynucleotidyl transferase (TdT)-mediated nick end-labelling (TUNEL), a significant increase in TUNEL + cells was demonstrated in decidua associated with partial (P = 0.0052) and complete (P = 0.0096) hydatidiform mole compared with normal early pregnancy. Co-labelling immunoperoxidase studies showed that the TUNEL + cells in both normal and molar pregnancies were not activated CD45RO+ immune cells, CD3+ T cells, CD56+ uterine natural killer (NK) cells or CD14+ CD68+ macrophages. Double immunohistochemical labelling with antiactive caspase-3 and leucocyte markers confirmed the lack of leucocyte apoptosis. Double immunostaining with anticytokeratin to detect trophoblast and M30 CytoDeath, which detects a neoepitope of cytokeratin 18 revealed after caspase-mediated cleavage, revealed apoptotic extravillous trophoblast cells within decidual tissue. We conclude that there is no evidence that apoptosis of decidual leucocytes plays a role in maintaining maternal tolerance in either normal or molar pregnancy.

Publication metadata

Author(s): Pongcharoen S, Bulmer JN, Searle RF

Publication type: Article

Publication status: Published

Journal: Clinical and Experimental Immunology

Year: 2004

Volume: 138

Issue: 2

Pages: 330-336

ISSN (print): 0009-9104

ISSN (electronic): 1365-2249

Publisher: Wiley-Blackwell

URL: http://dx.doi.org/10.1111/j.1365-2249.2004.02612.x

DOI: 10.1111/j.1365-2249.2004.02612.x

PubMed id: 15498045

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