Mucins Help to Avoid Alloreactivity at the Maternal Fetal Interface

During gestation, many different mechanisms act to render the maternal immune system tolerant to semi-allogeneic trophoblast cells of foetal origin, including those mediated via mucins that are expressed during the peri-implantation period in the uterus. Tumour- associated glycoprotein-72 (TAG-72) e...

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Main Authors: Arnela Redzovic, Gordana Laskarin, Marin Dominovic, Herman Haller, Daniel Rukavina
Format: Article
Language:English
Published: Hindawi Limited 2013-01-01
Series:Clinical and Developmental Immunology
Online Access:http://dx.doi.org/10.1155/2013/542152
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spelling doaj-f1d03d509086436b9c533a88f821e6ac2020-11-24T21:13:24ZengHindawi LimitedClinical and Developmental Immunology1740-25221740-25302013-01-01201310.1155/2013/542152542152Mucins Help to Avoid Alloreactivity at the Maternal Fetal InterfaceArnela Redzovic0Gordana Laskarin1Marin Dominovic2Herman Haller3Daniel Rukavina4Department of Physiology and Immunology, Medical Faculty, University of Rijeka, B. Branchetta 20, 51000 Rijeka, CroatiaDepartment of Physiology and Immunology, Medical Faculty, University of Rijeka, B. Branchetta 20, 51000 Rijeka, CroatiaDepartment of Physiology and Immunology, Medical Faculty, University of Rijeka, B. Branchetta 20, 51000 Rijeka, CroatiaDepartment of Obstetrics and Gynecology, Clinical Hospital, University of Rijeka, Kresimirova 42a, 51000 Rijeka, CroatiaDepartment of Physiology and Immunology, Medical Faculty, University of Rijeka, B. Branchetta 20, 51000 Rijeka, CroatiaDuring gestation, many different mechanisms act to render the maternal immune system tolerant to semi-allogeneic trophoblast cells of foetal origin, including those mediated via mucins that are expressed during the peri-implantation period in the uterus. Tumour- associated glycoprotein-72 (TAG-72) enhances the already established tolerogenic features of decidual dendritic cells with the inability to progress towards Th1 immune orientation due to lowered interferon (IFN)-γ and interleukin (IL)-15 expression. Mucine 1 (Muc 1) supports alternative activation of decidual macrophages, restricts the proliferation of decidual regulatory CD56+ bright natural killer (NK) cells, and downregulates their cytotoxic potential, including cytotoxic mediator protein expression. Removing TAG-72 and Muc 1 from the eutopic implantation site likely contributes to better control of trophoblast invasion by T cells and NK cells and appears to have important immunologic advantages for successful implantation, in addition to mechanical advantages. However, these processes may lead to uncontrolled trophoblast growth after implantation, inefficient defence against infection or tumours, and elimination of unwanted immunocompetent cells at the maternal-foetal interface. The use of mucins by tumour cells to affect the local microenvironment in order to avoid the host immune response and to promote local tumour growth, invasion, and metastasis confirms this postulation.http://dx.doi.org/10.1155/2013/542152
collection DOAJ
language English
format Article
sources DOAJ
author Arnela Redzovic
Gordana Laskarin
Marin Dominovic
Herman Haller
Daniel Rukavina
spellingShingle Arnela Redzovic
Gordana Laskarin
Marin Dominovic
Herman Haller
Daniel Rukavina
Mucins Help to Avoid Alloreactivity at the Maternal Fetal Interface
Clinical and Developmental Immunology
author_facet Arnela Redzovic
Gordana Laskarin
Marin Dominovic
Herman Haller
Daniel Rukavina
author_sort Arnela Redzovic
title Mucins Help to Avoid Alloreactivity at the Maternal Fetal Interface
title_short Mucins Help to Avoid Alloreactivity at the Maternal Fetal Interface
title_full Mucins Help to Avoid Alloreactivity at the Maternal Fetal Interface
title_fullStr Mucins Help to Avoid Alloreactivity at the Maternal Fetal Interface
title_full_unstemmed Mucins Help to Avoid Alloreactivity at the Maternal Fetal Interface
title_sort mucins help to avoid alloreactivity at the maternal fetal interface
publisher Hindawi Limited
series Clinical and Developmental Immunology
issn 1740-2522
1740-2530
publishDate 2013-01-01
description During gestation, many different mechanisms act to render the maternal immune system tolerant to semi-allogeneic trophoblast cells of foetal origin, including those mediated via mucins that are expressed during the peri-implantation period in the uterus. Tumour- associated glycoprotein-72 (TAG-72) enhances the already established tolerogenic features of decidual dendritic cells with the inability to progress towards Th1 immune orientation due to lowered interferon (IFN)-γ and interleukin (IL)-15 expression. Mucine 1 (Muc 1) supports alternative activation of decidual macrophages, restricts the proliferation of decidual regulatory CD56+ bright natural killer (NK) cells, and downregulates their cytotoxic potential, including cytotoxic mediator protein expression. Removing TAG-72 and Muc 1 from the eutopic implantation site likely contributes to better control of trophoblast invasion by T cells and NK cells and appears to have important immunologic advantages for successful implantation, in addition to mechanical advantages. However, these processes may lead to uncontrolled trophoblast growth after implantation, inefficient defence against infection or tumours, and elimination of unwanted immunocompetent cells at the maternal-foetal interface. The use of mucins by tumour cells to affect the local microenvironment in order to avoid the host immune response and to promote local tumour growth, invasion, and metastasis confirms this postulation.
url http://dx.doi.org/10.1155/2013/542152
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