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Published on: September 9, 2011
Antigen-presenting-cell function of interferon gamma-treated human gingival fibroblasts
Y Shimabukuro1, S Murakami, H Okada
1Department of Periodontology and Endodontology, Osaka University Faculty of Dentistry, Japan.
Insights
Human gingival fibroblasts (HGF) stimulated with IFN-gamma express HLA-DR but cannot activate naive T cells due to lack of CD80. However, these cells can stimulate primed T cells, suggesting a role in periodontal inflammation.
Area of Science:
- Immunology
- Cell Biology
- Periodontology
Background:
- Human gingival fibroblasts (HGF) are crucial in periodontal tissues.
- Antigen-presenting cells (APCs) play a key role in initiating immune responses.
- Interferon-gamma (IFN-gamma) is a cytokine involved in immune regulation.
Purpose of the Study:
- To investigate the antigen-presenting cell (APC) functions of human gingival fibroblasts (HGF) upon stimulation with IFN-gamma.
- To determine if IFN-gamma-treated HGF can stimulate T cell proliferation.
- To explore the potential role of HGF in immune responses within periodontal lesions.
Main Methods:
- Human gingival fibroblasts (HGF) were stimulated with IFN-gamma.
- Expression of HLA-DR and ICAM-1 on HGF was analyzed.
- T cell proliferation assays were performed using allo-reactive peripheral blood T cells (PBT) and primed CD4+ T cells.
- Detection of IL-1, PGE2, and CD80 expression on HGF.
- IFN-gamma mRNA levels in inflamed gingival tissue were measured.
Main Results:
- IFN-gamma stimulation induced HLA-DR and ICAM-1 expression on HGF, mimicking APC phenotype.
- IFN-gamma-treated HGF failed to induce proliferation of unprimed allo-reactive PBT.
- Lack of CD80 expression on IFN-gamma-treated HGF may explain their inability to stimulate naive T cells.
- IFN-gamma-treated HGF induced proliferation of primed allo-reactive CD4+ T cells in a HLA-DR-dependent manner.
- High levels of IFN-gamma mRNA were detected in inflamed gingival tissue.
Conclusions:
- IFN-gamma-stimulated HGF exhibit some APC characteristics but are ineffective at activating naive T cells.
- The absence of CD80 on IFN-gamma-treated HGF likely contributes to their limited APC function.
- IFN-gamma-treated HGF can stimulate pre-activated T cells, suggesting a role in modulating immune responses in periodontal inflammation.
- Locally secreted IFN-gamma may influence HGF function in inflammatory periodontal lesions.
Abstract:
The present study was carried out to examine the antigen-presenting cell (APC) functions of human gingival fibroblasts (HGF) elicited with IFN gamma. Stimulation of HGF with IFN gamma clearly induced HLA-DR expression and enhanced expression of intercellular adhesion molecule-1 (ICAM-1) on HGF. Despite the phenotypical resemblance of IFN gamma-treated HGF to so-called APC, HLA-DR positive HGF were unable to induce proliferation of allo-reactive peripheral blood T cells (PBT) isolated from different donors. The failure of IFN gamma-treated HGF to stimulate unprimed allo-reactive PBT was not due to the lack of production of IL-1 or the immunosuppressive effect of PGE2 from HGF. On the other hand, the fact that detectable expression of CD80, ligand for CD28, was not found on IFN gamma-treated HGF may at least in part explain the ineffective function of HGF as APC. Interestingly, IFN gamma-treated HGF induced proliferation of primed allo-reactive CD4+ T cells in a HLA-DR dependent manner, suggesting that IFN gamma-treated HGF may have the ability to stimulate pre-activated T cells. We then confirmed that high levels of IFN gamma mRNA were detectable in inflamed gingival tissue. Although it cannot be concluded from this study that HGF are incapable of effectively presenting antigenic peptides to autologous T cells bearing appropriate T cell receptors, present results suggest that HGF may be affected by locally-secreted IFN gamma and that the IFN gamma-stimulated HGF may play a role in regulating immune responsiveness in inflammatory periodontal lesions.
