Interactions of Immunomodulatory HLA-G with Immune Cells during Pregnancy and Endometriosis
The Major Histocompatibility Complex, the genetic region that encodes the
proteins responsible for tissue graft rejection, encodes MHC Class I (MHC-I) and MHC Class
II (MHC-II) glycoproteins.
Contrary to MHC-Ia proteins, nonclassical MHC-I (MHC-Ib) molecules are less polymorphic,
possess specific molecular motifs in their transmembrane domains and contain premature stop codons.
Immunological recognition of pathogens involves proteolysis of foreign
pathogen into peptides which are assembled on MHC-I and -II glycoproteins.
Interaction of MHC-I and MHC-II-peptide complexes with CD8 and CD4 T Cell Receptors,
respectively, leads to effector functions including removal of infected cells to clear the infection.
The fetal allograft must remain unharmed by the mother’s potentially hostile immune system
throughout the term. Several mechanisms have been reported which contribute
to immune tolerance to the fetus including the production
of Transforming Growth Factor beta 1 (TGF)-β1
and Interleukin-10 by T-regulatory cells, secretion of prolactin,
progesterone and gonadotropin by both fetal and endometrial cells,
secretion of immunosuppressive cytokines, chemokines,
and prostaglandins which dampen T lymphocyte proliferation.
An appropriate regulation of MHC class I genes at the maternal
fetal interface is critical for immunological acceptance of allogeneic conceptus.
Interactions of Immunomodulatory HLA-G with Immune Cells during Pregnancy and Endometriosis
Gynecol Obstet Res Open J. 2015; 2(4): 93-95. doi: 10.17140/GOROJ-2-121
