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Changes in expression of the CD 200 tolerance‐signaling molecule and its receptor ( CD 200R) by villus trophoblasts during first trimester missed abortion and in chronic histiocytic intervillositis
Author(s) -
Clark David A.,
Dmetrichuk Jennifer M.,
McCready Elizabeth,
DhesyThind Sukhbinder,
Arredondo Jorge L.
Publication year - 2017
Publication title -
american journal of reproductive immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.071
H-Index - 97
eISSN - 1600-0897
pISSN - 1046-7408
DOI - 10.1111/aji.12665
Subject(s) - trophoblast , cytotrophoblast , autocrine signalling , immunology , biology , placenta , andrology , receptor , fetus , medicine , pregnancy , genetics
Problem Expression of CD 200 at the feto‐maternal interface is associated with successful murine and human pregnancy. CD 200 binding to CD 200 receptors on lymphomyeloid cells suppresses inflammation and induces Tregs. CD 200 receptors are also expressed on mouse and human placental trophoblast cells. What is the expression of CD 200 and CD 200R in human missed abortions which have preserved Treg levels and in chronic histiocytic intervillositis ( CHI ) where maternal inflammatory cells cause IUGR ? Methods Immunohistiochemistry for CD 200, CD 200R, and Ki67 using human placental sections from missed abortions, term placenta, and CHI . PCR testing was done for trisomy in missed abortion. Results CD 200 and CD 200R were expressed by human villus trophoblasts from 2 weeks post‐implantation to term. Cytotrophoblast proliferation (Ki‐67 + count) decreased at term. In first trimester missed abortion cases, CD 200> CD 200R villus trophoblasts accompanied missed abortion of non‐trisomic male fetuses. CD 200 and Ki67 + trophoblast proliferation was preserved in CHI with maternal inflammatory cell infiltration but CD 200R was greatly decreased. Conclusion Residual CD 200 activity may prevent completion of abortions via induction of Treg cells. In CHI , infiltrating maternal effector T cells may block Treg induction. An autocrine role for CD 200‐ CD 200R interaction versus inhibition of soluble CD 200 by soluble CD 200R is discussed.