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Regulation of mitogen-driven lymphoreticular cell activation by human corneal cells and interleukin-1

N B Shams1, E M Huggins, M M Sigel

  • 1Department of Microbiology and Immunology, University of South Carolina School of Medicine, Columbia.

Cornea
|January 1, 1993
PubMed

Insights

Human corneal cells (FLE) inhibit immune cell DNA synthesis and activation. This immune regulation involves both cell-contact dependent mechanisms and soluble factors like prostaglandins, with Interleukin-1 (IL-1) playing a key role.

Area of Science:

  • Ophthalmology
  • Immunology
  • Cell Biology

Background:

  • Human corneo-scleral-conjunctival rims contain keratin-positive fibroblast-like epithelial cells (FLE).
  • Lymphoreticular cells (LRC), including thymocytes and splenocytes, are key components of the immune system.

Purpose of the Study:

  • To investigate the immunomodulatory effects of human corneal epithelial cells (FLE) on murine lymphoreticular cells (LRC).
  • To elucidate the mechanisms by which FLE cells and their secretions suppress LRC function.

Main Methods:

  • Assessing DNA synthesis in murine thymocytes and splenocytes stimulated with concanavalin A.
  • Measuring tetrazolium salt (MTT) reduction to evaluate cellular activation and mitochondrial activity.
  • Utilizing paraformaldehyde-fixed or irradiated FLE cells and their conditioned media.
  • Investigating the effects of interleukin-1 (IL-1) and indomethacin on FLE-mediated suppression.

Main Results:

  • FLE cells and their secretions significantly inhibited mitogen-induced DNA synthesis and cellular activation (reduced MTT reduction) in LRC.
  • Suppression was observed with live and fixed FLE cells, indicating both cell-contact dependent and soluble factor mechanisms.
  • Interleukin-1 (IL-1) reversed suppression by intact FLE cells.
  • Indomethacin blocked suppression by FLE-conditioned medium but not by whole FLE cells, suggesting prostaglandin involvement in soluble factor-mediated suppression.

Conclusions:

  • Corneal epithelial cells (FLE) possess potent immunoregulatory capabilities towards lymphoreticular cells (LRC).
  • FLE-mediated suppression of LRC function involves distinct mechanisms: cell-membrane-associated factors and soluble factors, potentially prostaglandins.
  • Interleukin-1 (IL-1) is implicated in regulating LRC function and may play a role in corneal immunity and inflammation.

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