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The endothelial cell as a regulator of T-cell function
C C Hughes1, C O Savage, J S Pober
1Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.
Immunological Reviews
|October 1, 1990
Summary
Endothelial cells (EC) present antigens and enhance T-cell activation by boosting interleukin-2 (IL-2) production. This occurs via cell contact, primarily through the CD2:LFA-3 interaction, and a secondary, CsA-resistant pathway.
Area of Science:
- Immunology
- Cell Biology
- T-cell activation
Background:
- Endothelial cells (EC) possess antigen-presenting capabilities, expressing MHC class I and II molecules.
- EC can activate T cells, including naive and memory populations, suggesting costimulatory functions.
- Interleukin-2 (IL-2) concentration is crucial for T-cell fate, influencing activation versus anergy.
Purpose of the Study:
- To investigate the role of EC in modulating T-cell IL-2 production.
- To elucidate the mechanisms by which EC act as costimulatory cells.
- To understand the pathways involved in EC-mediated T-cell activation.
Main Methods:
- Analysis of MHC molecule expression on EC.
- T-cell activation assays using peripheral blood mononuclear cells and purified T cells.
- Investigation of cell contact-dependent and independent pathways using blocking antibodies and immunosuppressive drugs.
Main Results:
- EC augment T-cell IL-2 production by 3- to 8-fold, enhancing T-cell proliferation.
- The primary mechanism involves cell contact via the CD2:LFA-3 ligand pair.
- A secondary, cyclosporine A (CsA)-resistant pathway was identified, but its ligands remain unknown.
Conclusions:
- EC are potent costimulatory cells that enhance T-cell responses by increasing IL-2 production.
- EC utilize both CD2:LFA-3-dependent and an additional CsA-resistant pathway for T-cell activation.
- These findings highlight EC's significant role in immune responses, including alloresponses.