Maternal T cells promote placental growth and prevent spontaneous abortion
Transplantation immunologists have long been intrigued by the natural allograft that results from normal mammalian pregnancy. Its general success contrasts with the rejection problems associated with most artifactual organ transplantation and raises intriguing questions concerning the nature of the...
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Published in | Immunology Letters Vol. 17; no. 4; pp. 297 - 302 |
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Main Author | |
Format | Book Review Journal Article |
Language | English |
Published |
Amsterdam
Elsevier B.V
01.04.1988
Elsevier |
Subjects | |
Online Access | Get full text |
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Summary: | Transplantation immunologists have long been intrigued by the natural allograft that results from normal mammalian pregnancy. Its general success contrasts with the rejection problems associated with most artifactual organ transplantation and raises intriguing questions concerning the nature of the mechanisms involved in that success. This area of research has recently taken on added momentum because it is now clear that immunological maneuvers can prevent recurrent spontaneous abortion in mice, horses and humans [1–3]. The purpose of this review is to discuss some of these recent developments, which lead to the surprising conclusion that maternal T cells, rather than being potentially detrimental to the fetal allograft, promote its growth and viability during normal pregnancy. This review will address these questions by considering: (a) the nature of the exposure of fetal alloantigens to the maternal circulation in the chimeric zone of the placenta; (b) the evidence for maternal immune recognition of the fetal alloantigens; and (c) the consequences of that recognition with respect to the prevention of spontaneous abortion. As in other areas of immunology the T cell emerges as the most important component of this immune recognition. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 ObjectType-Review-3 content type line 23 ObjectType-Feature-3 ObjectType-Review-1 |
ISSN: | 0165-2478 1879-0542 |
DOI: | 10.1016/0165-2478(88)90001-6 |