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Isolation of Leukocytes from the Murine Tissues at the Maternal-Fetal Interface
Published on: May 21, 2015
Immune cell profiling in normal pregnancy, partial and complete molar pregnancy
Zoltan Nagymanyoki1, Michael J Callahan, Mana M Parast
1Division of Gynecologic Oncology, New England Trophoblastic Disease Center, Department of Obstetrics and Gynecology, Brigham and Women's Hospital, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA.
Gynecologic Oncology
|September 20, 2007
Summary
Immune cells, including cytotoxic T cells (Tc) and natural killer (NK) cells, are more abundant in complete moles (CM) implantation sites than normal placenta. Regulatory T cells (Treg) may influence Tc activation in molar tissues.
Area of Science:
- Reproductive Immunology
- Gynecologic Oncology
- Cellular Immunology
Background:
- Cytotoxic T cells (Tc) and natural killer (NK) cells are implicated in controlling trophoblast invasion.
- Gestational trophoblastic diseases (GTD) involve abnormal trophoblast proliferation.
Purpose of the Study:
- To determine immune cell infiltration and antigen profiles in normal placenta (NP) and molar tissues.
- To explore relationships between immune cells in NP, partial moles (PM), and complete moles (CM) to understand GTD biology.
Main Methods:
- Immunolocalization of CD8, Granzyme B (GrB), and FoxP3 was performed on NP, PM, and CM tissues.
- Characterization of effector Tc cells (GrB+CD8+), GrB- Tc cells (GrB-CD8+), GrB+ NK cells (GrB+CD8-), and Treg cells (FoxP3+).
Main Results:
- Immune cell infiltration increased in the implantation site of NP, PM, and CM.
- CM showed significantly higher infiltration of effector Tc, GrB- Tc, GrB+ NK, and Treg cells compared to NP.
- Treg infiltration in the implantation site was observed only in PM and CM and positively correlated with Tc infiltration.
Conclusions:
- The cellular immune response in the implantation site is more vigorous in CM than in NP.
- Effector Tc and GrB+ NK cells are increased in CM implantation sites.
- Treg cells may play a role in negatively regulating T lymphocyte activation in CM.
