Premium
Antigen‐presenting‐cell function of interferon γ‐treated human gingival fibroblasts
Author(s) -
Shimabukuro Yoshio,
Murakami Shinya,
Okada Hiroshi
Publication year - 1996
Publication title -
journal of periodontal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.31
H-Index - 83
eISSN - 1600-0765
pISSN - 0022-3484
DOI - 10.1111/j.1600-0765.1996.tb00486.x
Subject(s) - cd80 , immune system , antigen , t cell , hepatocyte growth factor , immunology , cd28 , chemistry , cytotoxic t cell , receptor , biology , in vitro , medicine , cd40 , biochemistry
The present study was carried out to examine the antigen‐presenting cell (APC) functions of human gingival fibroblasts (HGF) elicited with IFNy. Stimulation of HGF with IFNy clearly induced HLA‐DR expression and enhanced expression of intercellular adhesion molecule‐1 (ICAM‐1) on HGF. Despite the phenotypical resemblance of IFNγ‐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 IFNγ‐treated HGF to stimulate unprimed allo‐reactive PBT was not due to the lack of production of IL‐1 or the immunosuppressive effect of PGE 2 from HGF. On the other hand, the fact that detectable expression of CD80, ligand for CD28, was not found on IFNy‐treated HGF may at least in part explain the ineffective function of HGF as APC. Interestingly, IFNγ‐treated HGF induced proliferation of primed allo‐reactive CD4 + T cells in a HLA‐DR dependent manner, suggesting that IFNγ‐treated HGF may have the ability to stimulate pre‐activated T cells. We then confirmed that high levels of IFNγ 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 IFNy and that the IFNγ‐stimulated HGF may play a role in regulating immune responsiveness in inflammatory periodontal lesions.