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RESEARCH REPORT |
1 Department of Periodontology,
2 Research Unit for Periodontal Disease,
3 Immunology Laboratory, and
4 Department of Oral Maxillofacial Surgery, Faculty of Dentistry, Chulalongkorn University, Henri Dunant Rd., Bangkok 10330, Thailand; and
5 Department of Immunology and Medicine, US Army Medical Component, Armed Forces Research Institute of Medical Sciences (AFRIMS), Bangkok, Thailand
* corresponding author, mrangsin{at}chula.ac.th
Interleukin (IL)-17 is present in inflammatory periodontal lesions, thus suggesting a role in mediating inflammation. We tested the hypothesis that IL-17, especially when combined with interferon (IFN)-
, may modulate the responses of human gingival fibroblasts (HGFs). IL-17 induced IL-8 and minimal intercellular adhesion molecule (ICAM)-1 expression. It had no effect on expression of HLA-DR, CD40, or the immune-suppressive enzyme indoleamine 2,3-dioxygenase (IDO). The effects of IL-17 on HGFs were compared with those of IFN-
. Unlike IL-17, IFN-
augmented the expression of HLA-DR, ICAM-1, and IDO, but not IL-8. Thus, IL-17 and IFN-
induce different HGF responses when administered separately. Interestingly, when IL-17 and IFN-
were combined, marked enhancement of ICAM-1, IL-8, and IDO expression by HGFs was observed. These findings suggest that IL-17, especially when combined with IFN-
, could play an important role in immune modulation through stimulation of HGFs in periodontal disease.
KEY WORDS: human gingival fibroblasts IL-17 IFN-
IL-8 IDO
Abbreviations: Interleukin (IL) T-helper (Th) human gingival fibroblasts (HGFs) indoleamine 2,3-dioxygenase (IDO) monoclonal antibodies (mAbs) intercellular adhesion molecule (ICAM)-1 interferon (IFN)-
tumor necrosis factor (TNF)-
mean fluorescence intensity (MFI)
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