Cutting edge: fasting-induced hypoleptinemia expands functional regulatory T cells in systemic lupus erythematosus.
Cutting edge: fasting-induced hypoleptinemia expands functional regulatory T cells in systemic lupus erythematosus.
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DOI：
10.4049/jimmunol.1102835
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发表时间：
2012-03-01
期刊：
影响因子：
--
通讯作者：
La Cava A
中科院分区：
文献类型：
--
作者：
Liu Y;Yu Y;Matarese G;La Cava A
禁食有利于预防和改善自身免疫性疾病包括系统性红斑狼疮（SLE）的临床表现。造成这些影响的机制尚不清楚。在禁食期间，循环中的瘦素水平显著降低，瘦素是一种具有促炎作用的脂肪因子。瘦素还抑制CD 4 + CD 25 + Foxp 3+调节性T细胞（TReg），已知其显著促进外周免疫耐受的机制。在这里，我们表明，在（NZB×NZW）F1狼疮易感小鼠中，禁食诱导的低瘦素血症诱导了功能性TReg的扩增，该扩增可被瘦素替代逆转。在瘦素缺乏的ob/ob小鼠和瘦素受体缺乏的db/db小鼠中缺乏这些作用表明了研究结果的特异性。这些观察结果有助于解释禁食对自身免疫的有益作用，并可用于SLE中基于瘦素的免疫干预。
Fasting is beneficial in the prevention and amelioration of the clinical manifestations of autoimmune diseases including systemic lupus erythematosus (SLE). The mechanisms responsible for these effects are not well understood. During fasting, there is a dramatic reduction of the levels of circulating leptin, an adipokine with proinflammatory effects. Leptin also inhibits CD4+CD25+Foxp3+ regulatory T cells (TReg), which are known to contribute significantly to the mechanisms of peripheral immune tolerance. Here we show that fasting-induced hypoleptinemia in (NZB×NZW)F1 lupus-prone mice induced an expansion of functional TReg that was reversed by leptin replacement. The specificity of the findings was indicated by the lack of these effects in leptin-deficient ob/ob mice and in leptin receptor-deficient db/db mice. These observations help to explain the beneficial effects of fasting in autoimmunity and could be exploited for leptin-based immune intervention in SLE.
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影响因子：
64.8
作者：
ZHANG, YY;PROENCA, R;FRIEDMAN, JM
通讯作者：
FRIEDMAN, JM
影响因子：
32.4
作者：
De Rosa, Veronica;Procaccini, Claudio;Matarese, Giuseppe
通讯作者：
Matarese, Giuseppe
影响因子：
64.5
作者：
Chen, H;Charlat, O;Morgenstern, JP
通讯作者：
Morgenstern, JP
影响因子：
4.4
作者：
Scalapino, Kenneth J.;Tang, Qizhi;Daikh, David I.
通讯作者：
Daikh, David I.
DOI：
10.1073/pnas.75.3.1500
发表时间：
1978-01-01
影响因子：
11.1
作者：
FERNANDES, G;FRIEND, P;GOOD, RA
通讯作者：
GOOD, RA