Modulation of Antigenic Phenotype in Cultured Human Osteoblast-like Cells by FGFb, TGF beta 1, PDGF-BB, IL-2, IL-1 beta , LPS and IFN gamma
Background/Aims: Recent reports demonstrated that osteoblast-like cells can also exert activities directly associated with the immune system (cytokine synthesis, antigen presentation, phagocytosis and stimulation of T lymphocytes). The present study aimed to analyze the effect of Transforming growth...
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Published in | Bioscience reports Vol. 26; no. 4; pp. 281 - 289 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
01.08.2006
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Online Access | Get full text |
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Summary: | Background/Aims: Recent reports demonstrated that osteoblast-like cells can also exert activities directly associated with the immune system (cytokine synthesis, antigen presentation, phagocytosis and stimulation of T lymphocytes). The present study aimed to analyze the effect of Transforming growth factor beta 1 (TGF beta 1), Fibroblast growth factor basic (FGFb), Platelet-derived growth factor-BB (PDGF-BB), Interleukin-1 beta (IL-1 beta ), Interleukin-2 (IL-2), Lipopolysaccharide (LPS) and Interferon- gamma (IFN gamma ) on the expression on osteoblast-like cells of antigens involved in antigen presentation. Methods: Flow cytometry was used to investigate whether the growth factors FGFb, TGF beta 1, PDGF-BB, IL-2, IL-1 beta , LPS and IFN gamma modulate the expression on cultured human osteoblast-like cells of different antigens involved in antigen-presentation and T cell activation. Results: TGF beta 1 treatment significantly reduced the expression of CD54 and CD86. IL-1 beta treatment significantly enhanced the expression of CD54, CD86 and HLA-DR. LPS and IFN gamma treatments produced a major increase in CD54, CD80, CD86 and HLA-DR expression. Expression of these antigen-presenting molecules was not significantly modified by FGFb, PDGF-BB or IL-2 treatment. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0144-8463 |
DOI: | 10.1007/s10540-006-9022-z |