Major histocompatibility complex (MHC)-mediated immune regulation of decidual leukocytes at the fetal–maternal interface

Received 27 August 2009; received in revised form 3 December 2009; accepted 20 January 2010. published online 08 March 2010.

Abstract

Self and non-self recognition is the key mechanism by which the immune system determines whether or not to mount an immune response. During pregnancy the maternal immune system must tolerate the persistence of non-self semi-allogeneic fetal cells in the maternal tissue. Although many mechanisms have been shown to contribute to the prevention of a destructive maternal immune response to fetal cells, the immune acceptance of the allogeneic fetus in pregnancy largely remains an immunological paradox (Billingham et al., 1953). The aim of this review is to describe the expression of the polymorphic histocompatibility antigens at the fetal–maternal interface, their interaction with maternal leukocytes and their possible roles in immune regulation at the fetal–maternal interface during human pregnancy.

Abbreviations: EVT, extravillous trophoblast, HLA, human leukocyte antigen, KIR, killer immunoglobulin-like receptor, MHC, major histocompatibility complex, mHag, minor histocompatibility antigen, TCR, T cell receptor

Keywords: HLA, Human, Decidua, T cells, NK cells

a Department of Immunohematology and Blood Transfusion, Leiden University Medical Center, Leiden, The Netherlands

b Department of Obstetrics, Leiden University Medical Center, Leiden, The Netherlands

Corresponding author at: Leiden University Medical Center, Department of Immunohematology and Blood Transfusion E3Q, PO Box 9600, 2300 RC Leiden, The Netherlands.

1 Current work address: Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA, USA.

PII: S0165-0378(10)00040-9

doi:10.1016/j.jri.2010.01.005

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