Dec, 2000
Tumor Necrosis Factor-α (TNF-α)-Induced and Interleukin-1β (IL-1β)-Induced Shedding of TNF Receptors from Gingival Fibroblasts
Journal of Interferon & Cytokine Research
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- Volume
- 20
- Number
- 12
- First page
- 1077
- Last page
- 1082
- Language
- English
- Publishing type
- Research paper (scientific journal)
- DOI
- 10.1089/107999000750053744
- Publisher
- Mary Ann Liebert Inc
Tumor necrosis factor-alpha (TNF-alpha) exerts its functions by binding two different receptors (TNFR55 and TNFR75), Both TNFR55 and TNFR75 exist in cell-associated and soluble forms. Soluble TNF receptors (sTNFR), sTNFR55 and sTNFR75, are proteolytically shed upon inflammatory stimuli and then modulate various TNF-alpha bioactivities. As human gingival fibroblasts (HGF) can be potential targets for TNF-alpha in inflamed gingiva, we hypothesized that HGF partially modulate the cellular responses to TNF-alpha by regulating their own TNFR. In this study, the kinetics of expression of cell-associated and soluble forms of both receptors from cultured HGF in response to proinflammatory cytokines TNF-alpha and interleukin-1 beta (IL-1 beta) were investigated in vitro. Both TNF-alpha and IL-1 beta upregulated the gene expression of TNFR75 and did not affect that of TNFR55. TNF-alpha and IL-1 beta decreased binding of [I-125]TNF-alpha to HGF. Moreover, TNF-alpha and IL-1 beta upregulated the release of sTNFR75 from HGF but not that of sTNFR55, These results suggest that HGF under inflammatory conditions may contribute to the inactivation of circulating TNF-a through the preferential induction and shedding of TNFR75.
- Link information
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- DOI
- https://doi.org/10.1089/107999000750053744
- CiNii Articles
- http://ci.nii.ac.jp/naid/80012019910
- PubMed
- https://www.ncbi.nlm.nih.gov/pubmed/11152574
- Web of Science
- https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000166111400006&DestApp=WOS_CPL
- URL
- http://www.liebertpub.com/doi/pdf/10.1089/107999000750053744
- ID information
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- DOI : 10.1089/107999000750053744
- ISSN : 1079-9907
- eISSN : 1557-7465
- CiNii Articles ID : 80012019910
- ORCID - Put Code : 47542648
- Pubmed ID : 11152574
- Web of Science ID : WOS:000166111400006