Abstract
We investigated the mechanism and impact of various inflammatory stimuli on dendritic cell (DC)-gingival fibroblast (GF) adhesion. Human immature (im) DCs were generated from monocytes by culturing with interleukin (IL)-4 and granulocyte macrophage-colony stimulating factor (GM-CSF). GFs were outgrown from the human gingival specimen. DCs were co-cultured with GFs with/without pretreatment with various stimuli. Adhered cells were measured by fluorometer. Expression of adhesion molecules was analyzed by flow cytometry. Pretreatment of GFs with tumor necrosis factor (TNF)-α, interferon (IFN)-γ, and Escherichia coli (Ec) lipopolysaccharides (LPS) significantly increased the adhesion to imDCs and enhanced intercellular adhesion molecule (ICAM)-1 expression. A signifi-cantly increased DC-GF adhesion was also observed when imDCs were pretreated with Ec LPS, Porphyromonas gingivalis (Pg) fimbriae, and peptideglycan but not with Pg LPS. Expression of LFA-1 and Mac-1 on DCs was not altered by the pretreatment with these stimuli. However, LFA-1 and Mac-1 blockade of imDC signifi cantly reduced the adhesion to TNF-α-stimulated GFs. These results showed that inflammatory stimuli increased the imDC-GF adhesion via lymphocyte function- associated antigen (LFA)-1/Mac-1-ICAM-1 ligation. Adhesion of DC to GFs may be important not only for the localization of DCs in the inflammatory periodontal lesion, but also for the modulation of immune responses.
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Minamibuchi, M., Nemoto, E., Kanaya, S., Ogawa, T., Simauchi, H. (2007). Inflammatory stimuli regulate the binding of gingival fibroblasts to dendritic cells via integrin β2. In: Watanabe, M., Okuno, O., Sasaki, K., Takahashi, N., Suzuki, O., Takada, H. (eds) Interface Oral Health Science 2007. Springer, Tokyo. https://doi.org/10.1007/978-4-431-76690-2_37
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DOI: https://doi.org/10.1007/978-4-431-76690-2_37
Publisher Name: Springer, Tokyo
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