B cells activated in the presence of Th1 cytokines inhibit osteoclastogenesis.

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Choi, Youngnim; Kim, Jeong Jae

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Korean Society of Medical Biochemistry
Exp Mol Med. 2003;35(5):385-392
B lymphocyte subsetscytokinesinterferon type IIinterleukin-2osteoclastsTh1 cells
Host immune response has been considered as an important disease-modifying factor of periodontitis, however, which immune cell(s) or factor(s) are involved in the destruction of periodontium remains unclear. Previously, we reported that osteoclastogenesis is enhanced by activated B cells but suppressed by activated CD8+ T cells. We present new data that B cells activated in the presence of Th1 cytokines inhibit osteoclastogenesis. Purified murine B cells were activated with anti-IgD mAb, IL-4, and anti-CD40 mAb, in the absence (BTh2) or presence of Th1 cytokines, either IL-2 (BIL-2) or IFN-gamma (BIFN-gamma). Each activated B cell population was co-cultured with RAW264.7 cells in the presence of soluble receptor activator of NF-kappaB ligand (sRANKL), and the effect on osteoclastic differentiation was evaluated. While BTh2 increased osteoclastogenesis, BIL-2 and BIFN-gamma suppressed it profoundly. To verify the mediating molecule(s), we analyzed cytokine profiles of the activated B cells. Compared to BTh2, BIL-2 expressed increased amount of IFN-gamma and BIFN-gamma expressed decreased amounts of IL-4, IL-5, and IL-10. IFN-gamma was a key negative regulator of osteoclastic differentiation, and mediated the inhibition by BIL-2. These results suggest that Th1 cytokines may have new important roles in resistance to periodontitis, acting directly on osteoclasts or indirectly through B cells.
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College of Dentistry/School of Dentistry (치과대학/치의학대학원)Dept. of Dentistry (치의학과)Journal Papers (저널논문_치의학과)
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