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Related Experiment Videos

Selective prothymocyte targeting by prenatal diethylstilbesterol exposure

S D Holladay1, B L Blaylock, C E Comment

  • 1Developmental and Reproductive Toxicology Group, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709.

Cellular Immunology
|November 1, 1993
PubMed
Summary

Prenatal exposure to diethylstilbestrol (DES) severely impacts the developing immune system, causing thymic atrophy by targeting fetal liver lymphocyte stem cells. This highlights estrogenic hormone sensitivity during development.

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Area of Science:

  • Immunology
  • Developmental Biology
  • Endocrinology

Background:

  • Estrogens modulate immune responses.
  • Diethylstilbestrol (DES), a synthetic estrogen, causes thymic atrophy in adult animals.
  • Prenatal exposure to endocrine-disrupting chemicals can impact developing immune systems.

Purpose of the Study:

  • To investigate the effects of prenatal diethylstilbestrol (DES) exposure on the developing immune system, specifically thymic cellularity and fetal liver hematopoietic stem cells.
  • To determine if prenatal DES exposure causes greater thymic atrophy than adult exposure.
  • To identify potential targets of DES within the fetal immune system.

Main Methods:

  • Histological analysis of thymic cellularity in prenatal DES-exposed mice.

Related Experiment Videos

  • Flow cytometry to analyze cell surface antigens (CD4, CD8, CD44, Mac-1, CD45R) in fetal liver hematopoietic subpopulations.
  • Quantification of terminal deoxynucleotidyl transferase (TdT) in fetal liver cells.
  • Fetal liver cell reconstitution assays in irradiated hosts.
  • Measurement of estrogen receptors in fetal liver prelymphoid cells.

    • Main Results:

    • Prenatal DES exposure resulted in more severe thymic atrophy compared to adult exposure.
    • DES exposure caused minimal alterations in thymocyte maturation (CD4, CD8 expression).
    • DES selectively reduced fetal liver prothymocytes expressing terminal deoxynucleotidyl transferase (TdT).
    • DES-treated fetal liver showed impaired ability to repopulate the thymus in irradiated hosts.
    • Fetal liver prelymphoid cells exhibited estrogen-specific receptors.

    Conclusions:

    • The developing immune system, particularly fetal lymphocyte stem cells, is highly sensitive to estrogenic hormones like DES.
    • Prenatal DES-induced thymic atrophy appears to result from specific targeting of fetal liver prothymocytes, not direct thymocyte injury.
    • Estrogen-mediated thymic atrophy may stem from alterations in the lymphocyte stem cell population responsible for thymus colonization.