T cells are able to promote lipopolysaccharide-induced bone resorption in mice in the absence of B cells
Background and Objective: T cells and their cytokines are believed to be key factors in periodontal disease and bone resorption. We previously showed that T cells transferred to nude mice were related to inflammatory bone resorption in vivo. However, it has not been clarified whether T cells can in...
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Veröffentlicht in: | Journal of periodontal research 2008-10, Vol.43 (5), p.549-555 |
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Sprache: | eng |
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Zusammenfassung: | Background and Objective: T cells and their cytokines are believed to be key factors in periodontal disease and bone resorption. We previously showed that T cells transferred to nude mice were related to inflammatory bone resorption in vivo. However, it has not been clarified whether T cells can induce bone resorption in the absence of B cells. In this study, we therefore investigated the ability of T cells to induce bone resorption without B cells, using both T cell‐ and B cell‐deficient mice with severe combined immune deficiency (SCID).
Material and Methods: Escherichia coli lipopolysaccharide (LPS) was injected into the gingivae of SCID mice reconstituted by T cells (SCID + T mice). Wild‐type C.B‐17 mice and SCID mice were used as control animals. Alveolar bone resorption and production of cytokines in the gingivae were then compared histopathologically and immunohistologically.
Results: The degree of bone resorption in SCID + T mice was significantly greater than that in SCID mice but less than that in wild‐type mice. The same tendency was found for expression of receptor activator of nuclear factor κB ligand. The number of interferon‐γ‐positive cells in SCID + T mice was the highest of the three groups. In contrast, interleukin‐4‐positive cells were detected in wild‐type mice but not in SCID + T and SCID mice.
Conclusion: The results suggest that T cells are able to promote LPS‐induced bone resorption in the absence of B cells. The expressions of cytokines in the presence of B cells are quite different. |
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ISSN: | 0022-3484 1600-0765 |
DOI: | 10.1111/j.1600-0765.2008.01083.x |