Downregulation of ILT4+ dendritic cells in recurrent miscarriage and recurrent implantation failure

Am J Reprod Immunol. 2018 Oct;80(4):e12998. doi: 10.1111/aji.12998. Epub 2018 Jun 14.

Abstract

Problem: The role of ILT4+ DCs in healthy fertile controls and patients with recurrent miscarriages (RM) and recurrent implantation failure (RIF) is unclear.

Method of study: We studied the expression of ILT4 from peripheral blood and endometrial samples from healthy controls and patients with RM and RIF by flow cytometry and immunohistochemistry analysis. Endometrial Foxp3 expression was also investigated using immunohistochemistry.

Results: In peripheral blood, there was a significant increase in the percentage of ILT4+ DCs in healthy fertile controls compared with patients with RM and RIF. The presence of ILT4+ DC is even more prominent in the endometrium of healthy fertile controls compared with patients with RM and RIF. Moreover, there was a strong correlation between the number of ILT4+ cells and Foxp3+ Tregs in healthy fertile controls, but not in patients with RM and RIF.

Conclusion: Our data indicate that ILT4+ DCs play an important role in the maintenance of immune tolerance during pregnancy, probably through the induction of Foxp3+ Treg cells, a process which is impaired in RM and RIF.

Keywords: RIF; RM; Foxp3+ Treg; ILT4+ DCs.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Abortion, Habitual / immunology*
  • CD4 Lymphocyte Count
  • Cytokines / blood
  • Dendritic Cells / metabolism*
  • Embryo Implantation / physiology*
  • Endometrium / cytology
  • Endometrium / metabolism*
  • Female
  • Forkhead Transcription Factors / metabolism
  • Humans
  • Immune Tolerance / immunology
  • Membrane Glycoproteins / metabolism*
  • Pregnancy
  • Receptors, Immunologic / metabolism*
  • T-Lymphocytes, Regulatory / immunology

Substances

  • Cytokines
  • FOXP3 protein, human
  • Forkhead Transcription Factors
  • LILRB2 protein, human
  • Membrane Glycoproteins
  • Receptors, Immunologic