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- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2017.1
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- 1 - 13 (13page)
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Resveratrol, an anti-inflammatory agent, can inhibit pro-inflammatory mediators by activating Sirt1, which is a class III histone deacetylase. However, whether resveratrol can regulate inhibitory or anti-inflammatory molecules has been less studied. FcγRIIB, a receptor for IgG, is an essential inhibitory receptor of B cells for blocking B-cell receptor-mediated activation and for directly inducing apoptosis of B cells. Because mice deficient in either Sirt1 or FcγRIIB develop lupus-like diseases, we investigated whether resveratrol can alleviate lupus through FcγRIIB. We found that resveratrol enhanced the expression of FcγRIIB in B cells, resulting in a marked depletion of plasma cells in the spleen and notably in the bone marrow, thereby decreasing serum autoantibody titers in MRL/lpr mice. The upregulation of FcγRIIB by resveratrol involved an increase of Sirt1 protein and deacetylation of p65 NF-κB (K310). Moreover, increased binding of phosphor-p65 NF-κB (S536) but decreased association of acetylated p65 NF-κB (K310) and phosphor-p65 NF-κB (S468) to the − 480 promoter region of Fcgr2b gene was responsible for the resveratrol-mediated enhancement of FcγRIIB gene transcription. Consequently, B cells, especially plasma cells, were considerably reduced in MRL/lpr mice, leading to improvement of nephritis and prolonged survival. Taken together, we provide evidence that pharmacological upregulation of FcγRIIB expression in B cells via resveratrol can selectively reduce B cells, decrease serum autoantibodies and ameliorate lupus nephritis. Our findings lead us to propose FcγRIIB as a new target for therapeutic exploitation, particularly for lupus patients whose FcγRIIB expression levels in B cells are downregulated.
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참고문헌 (27)
참고문헌 신청
Blanchard OL / 2015 / Trans
Bolland S / 2000 / Spontaneous autoimmune disease in FcγRIIBdeficient mice results from strain-specific epistasis / Immunity 13 : 277 ~ 285
Chacko GW / 1996 / Negative signaling in B lymphocytes induces tyrosine phosphorylation of the 145-kDa inositol polyphosphate 5-phosphatase, SHIP / J Immunol 157 : 2234 ~ 22
Consiglio CR / 2014 / SIRT1 promoter polymorphisms as clinical modifiers on systemic lupus erythematosus / Mol Biol Rep 41 : 4233 ~ 4239
Daeron M / 2014 / Fc receptors as adaptive immunoreceptors / Curr Top Microbiol Immunol 382 : 131 ~ 164
Bolland S / 2000 / Spontaneous autoimmune disease in FcγRIIBdeficient mice results from strain-specific epistasis / Immunity 13 : 277 ~ 285
Chacko GW / 1996 / Negative signaling in B lymphocytes induces tyrosine phosphorylation of the 145-kDa inositol polyphosphate 5-phosphatase, SHIP / J Immunol 157 : 2234 ~ 22
Consiglio CR / 2014 / SIRT1 promoter polymorphisms as clinical modifiers on systemic lupus erythematosus / Mol Biol Rep 41 : 4233 ~ 4239
Daeron M / 2014 / Fc receptors as adaptive immunoreceptors / Curr Top Microbiol Immunol 382 : 131 ~ 164
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